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ZENG Jing-jing XU Xiao-xiao SHI Han-qing XU Guang-yu JIN Qi-ke RUAN Yong-xue REN Fang-fang XIE Zuo-yi LI Lei 《园艺学报》2021,36(12):2113-2122
AIM To investigate the effect of cyanidin （Cyn） on pressure overload-induced cardiac remodeling and the underlying mechanism. METHODS Six-week-old male C57BL/6 mice （n =120） were divided into 4 groups： sham group （n =20）, sham+Cyn group （n =20）, transverse aortic constriction （TAC） group （n =40） and TAC+Cyn group （n =40）. The model of cardiac chronic pressure overload was induced by TAC, and the first day of TAC was defined as day 0. The animals in sham+Cyn group and TAC+Cyn group were treated with Cyn dissolved in DMSO and normal saline （5 mg·kg-1·d-1） for 5 d before TAC, while the animals in sham group and TAC group were treated with the same amount of DMSO and normal saline. Four weeks after TAC, the survival rate of the animals in each group was analyzed, the heart function of the mice was measured by ultrasound echocardiography, and the heart weight/body weight and lung weight/body weight were calculated. The cross-sectional area of the cardiomyocytes was measured by wheat germ agglutinin staining and hematoxylin-eosin staining. The degree of cardiac oxidative stress was evaluated by dihydroethidium staining and measurement of superoxide dismutase （SOD） and malondialdehyde （MDA） levels. The cardiomyocyte apoptosis was detected by TUNEL method. The mRNA expression levels of atrial natriuretic peptide （ANP）, brain natriuretic peptide （BNP） and β-myosin heavy chain （β-MHC） were detected by RT-qPCR, and the protein expression levels of Bax, Bcl-2, optic atrophy protein 1 （OPA1） and dynamin-related protein 1 （Drp1） were determined by Western blot. The mitochondrial morphological changes were observed by transmission electron microscopy. RESULTS Compared with TAC group, the survival rate of the mice in TAC+Cyn group was significantly increased （P <0.05）, the myocardial apoptosis, the cross-sectional area of myocardial cells, the heart weight/body weight, the lung weight/body weight, the level of reactive oxygen species and the MDA content were decreased （P <0.05）, and the SOD was activated （P <0.05）. M-mode ultrasound tests showed that Cyn treatment significantly increased left ventricular ejection fraction and left ventricular fractional shortening in the mice after TAC （P <0.05）, while left ventricular end-diastolic diameter and left ventricular posterior wall thickness in diastole were reduced （P <0.05）. Transmission electron microscopic observation showed that the number of myocardial mitochondria was increased and the mitochondrial area was decreased after TAC （P <0.05）, while treatment with Cyn increased the area of myocardial mitochondria and decreased the mitochondrial number （P <0.05）. Compared with sham group, the protein level of OPA1 in TAC group was significantly reduced （P <0.05）, while treatment with Cyn significantly increased the protein level of OPA1. CONCLUSION Cyanidin significantly increases the survival rate, improves the cardiac function and attenuates the cardiac remodeling of the mice after TAC. The mechanism may be related to the inhibition of myocardial mitochondrial OPA1 cleavage and the promotion of mitochondrial fusion. 相似文献
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AIM To analyze the regulatory effect of quercetin （QUE） on PTEN-induced putative kinase 1 （PINK1）/parkin mitochondrial autophagy pathway, and to explore the mechanism of quercetin in relieving cerebral ischemia/reperfusion （I/R） injury. METHODS Sixty SD male rats were randomly divided into sham operation group, model group （I/R group）, QUE group,3-methyladenine （3-MA） group and QUE+3-MA group. Administration started in each group 3 days before modeling, once a day, at 30 min after the last administration,except sham group, the other groups used 4-vessel blockage method to establish the whole brain I/R model. On the day after modeling, the neural function was evaluated by neuropathy disability score （NDS）. The volume of cerebral infarction was measured by 2,3,5-triphenyltetrazolium chloride （TTC） staining. The morphological changes of mitochondria in hippocampus were observed by transmission electron microscopy. The contents of interleukin-6 （IL-6） and tumor necrosis factor-α （TNF-α） in hippocampus were measured by ELISA. The activity of superoxide dismutase （SOD） and contents of malondialdehyde （MDA） in hippocampus were detected by xanthine oxidase method, thiobarbituric acid condensation method. Western blot was used to detect the proteinex pression of PINK1, parkin and LC3-II in brain tissue. RESULTS Compared with sham group, the hippocampus of the rats in I/R group and QUE+3-MA group showed swelling of mitochondria, destruction or disappearance of internal crista and other pathological damage,also the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA, the protein expression levels of PINK1, parkin and LC3-II were increased （P <0.05）, while NDS score and activity of SOD were decreased （P <0.05）. Compared with I/R group and QUE+3-MA group, the pathological damage degree of hippocampus in QUE group was reduced, the volume of cerebral infarction, the contents of IL-6, TNF-α and MDA were decreased （P <0.05）, the proteinexpression levels of PINK1, parkin and LC3-II, and NDS score and activity of SOD were increased （P <0.05）.The above indexes in 3-MA group were opposite to QUE group. No significant difference in the above indexes between I/R group and QUE+3-MA group was observed （P >0.05）. CONCLUSION Quercetin activates mitochondrial autophagy and reduces cerebral I/R by regulating the expression of PINK1/parkin pathway proteins. 相似文献
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AIM To investigate the effect of scutellarin （SCU） on oxidative stress and apoptosis induced by lipopolysaccharide （LPS） in human glomerular epithelial cells and its mechanism. METHODS Human glomerular epithelial cells were cultured in vitro , and were treated with LPS （1.0 mg/L） to establish a cell injury model. The cells were divided into normal control （NC） group, LPS group, NC+SCU group, LPS+SCU group, LPS+miR-NC group, LPS+microRNA-7-5p （miR-7-5p） group, LPS+SCU+anti-miR-NC group and LPS+SCU+anti-miR-7-5p group. Cell viability was detected by CCK-8 assay. Apoptosis was detected by flow cytometry. The intracellular malondialdehyde （MDA） content and superoxide dismutase （SOD） activity, and lactate dehydrogenase （LDH） activity in the cell culture supernatant were determined by kit. RT-qPCR was used to detect the expression level of miR-7-5p. RESULTS Compared with NC group, the cell viability, miR-7-5p expression and SOD activity in LPS group were significantly reduced, and the apoptotic rate, MDA content and LDH activity were significantly increased （P <0.05）. Compared with LPS group, the cell viability, miR-7-5p expression and SOD activity in LPS+SCU group were significantly increased, and the apoptotic rate, MDA content and LDH activity were significantly reduced （P <0.05）. Compared with LPS+miR-NC group, the cell viability and SOD activity in LPS+miR-7-5p group were significantly increased, and the apoptotic rate, MDA content and LDH activity were significantly reduced （P <0.05）. Compared with LPS+SCU+anti-miR-NC group, the cell viability and SOD activity in LPS+SCU+anti-miR-7-5p group were significantly reduced, and the apoptotic rate, MDA content and LDH activity were significantly increased （P <0.05）. CONCLUSION Scutellarin inhibits LPS-induced oxidative stress damage and apoptosis in glomerular epithelial cells via up-regulating miR-7-5p expression. 相似文献
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XIE Yi-lian YANG Nai-bing WANG Li-ping XUAN Yan-yan WU Yi-yi QIAN Guo-qing SHI Jie-jun SHI Guang-xia LI Guo-xiang 《园艺学报》2020,36(5):860-864
AIMTo investigate the effect of curcumin (CUR) on autophagy of hepatovyte in rats with lipopolysaccharide (LPS)/D-galactosamine (D-GalN)-induced acute liver injury (AHI). METHODSThe healthy male Sprague-Dawley (SD) rats were randomized into the control group,AHI group,CUR group, 3-methy-ladenine (3-MA) group and 3-MA+CUR group, with 6 rats in each group. AHI was induced with an intraperitoneal injection of LPS and D-GalN. Liver function was tested 12 h after LPS/D-GalN treatment. Pathological changes of liver tissues were analyzed by HE staining.The amount of autophagic bodies were observed by transmission electron microscopy. The protein levels of autophagy related-proteins LC3 and beclin 1 in livers were detected by Western blot. ELISA were used to examine the serum levels of tumor necrosis factor-α (TNF-α). RESULTSCompared with control group, the serum level of alanine aminotransferase (ALT) and asparated aminotransferase (AST) were significantly increased, hepatic pathological damage were aggravated and serum TNF-α level was significantly increased in AHI group, while the autophagic bodies and the protein levels of LC3 and beclin 1 were increased (P <0.01). Compared with AHI group, the serum level of ALT and AST were significantly decreased, hepatic pathological damage were attenuated and serum TNF-α level was significantly reduced (P? <0.05), while the autophagic bodies and the protein levels of LC3 and beclin 1 were significantly increased in CUR group (P <0.01). Compared with CUR group, the serum level of ALT and AST were significantly increased, hepatic pathological damage were aggravated and serum level of TNF-α was significantly increased in 3-MA group and 3-MA+CUR group, while the autophagic bodies and the protein levels of LC3 and beclin 1 were decreased (P <0.01). CONCLUSION Curcumin protects rats against LPS/D-GalN-induced liver injury, partially due to activation of hepatocyte autophagy in livers. 相似文献
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GAO Hui ZHOU Zhuo-lin LOU Guo-qiang ZHANG Jing-jing WU Yuan-ling HUANG Dan-na WU Yi-ming WANG wan-tie 《园艺学报》2000,36(10):1825-1832
AIM To investigate the regulatory effect of retinoic acid X receptor （RXR） on autophagy induced by hypoxia/reoxygenation （H/R） in rat alveolar type Ⅱ epithelial cells （AEC Ⅱ） and its molecular mechanism. METHODS AEC Ⅱ were cultured in normoxia. The cells growing to logarithmic growth phase were randomly divided into 5 groups： （1） control （Con） group： cells were cultured for 30 h under normal operation; （2） H/R group： cells were cultured in hypoxia condition for 6 h and then in reoxygenation condition for 24 h; （3） DMSO group： cells were pretreated 1.5 h with medium containing less than 0.1% DMSO before modeling, and the rest were treated the same as the H/R group; （4） 9-cis -retinoic acid （9-RA） group： cells were pretreated for 1 h with 9-RA （100 nmol/L） before hypoxia; （5） HX531 group： cells were treated with 9-RA （100 nmol/L） for 0.5 h, then treatment with HX531 （2.5 μmol/L） for 1 h. CCK-8 assay was used to detect the cell viability. Immunofluorescence staining was used to observe the expression of RXRα. Transmission electron microscope was used to observe the changes of intracellular ultrastructure, and the mRNA expression of adenosine AMP-activated protein kinase （AMPK）, beclin 1, LC3, mammalian target of rapamycin （mTOR） and P62 was detected by RT-PCR. Western blot was used to detected the protein levels of p-AMPK, beclin 1, LC3-Ⅱ, p-mTOR and P62. RESULTS Compared with Con group, the cell viability in H/R, DMSO, 9-RA and HX531 groups were significantly decreased. The mRNA expression of AMPK, beclin 1 and LC3 was significantly increased, and the protein levels of p-AMPK, beclin 1 and LC3-Ⅱ were also increased. The mRNA expression of mTOR and P62 was decreased, and the protein levels of p-mTOR and P62 were also decreased （P <0.05）. The cell injury in 9-RA group was alleviated and autophagy level was significantly lower than that in H/R, DMSO and HX531 groups （P <0.05）, and no significant difference among H/R, DMSO and HX531 groups was observed （P >0.05）. CONCLUSION H/R induces autophagy of AEC Ⅱ. Activating RXR reduce the damage of AEC Ⅱ cells induced by H/R, and its mechanism may be related to the inhibition of autophagy. 相似文献
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AIM To investigate the effects of astragaloside on the levels of sex hormone and oxidative stress in rats with polycystic ovary syndrome （PCOS）. METHODS Female SD rats （n =60） were randomly divided into normal control group, model group, Diane-35 （0.339 2 mg/kg） group, low dose astragaloside （12.5 mg/kg） group and high dose astragaloside （50 mg/kg） group, with 12 rats in each group. The PCOS model was induced by letrozole （1 mg/kg）, which was administered by gavage once a day for 3 weeks. After administration, the estrus cycle of the rats was observed by vaginal smear, and the ovarian index was calculated. HE staining was used to observe the histopathological changes of the ovaries. Serum levels of the sex hormones testosterone （T）, estradiol （E2）, luteinizing hormone （LH） and follicle-stimulating hormone （FSH） were measured by ELISA. The levels of superoxide dismutase （SOD）, malondialdehyde （MDA） and glutathione peroxidase （GSH-Px） in serum and ovarian tissue were detected by colorimetry, and the protein levels of steroidogenetic acute regulatory protein （StAR） and apoptosis-related proteins cleaved caspase-3, Bax and Bcl-2 in ovarian tissue were detected by Western blot. RESULT Compared with control group, the oestrous cycle of the rats in model group was disorder, and the ovarian index was increased, ovary was polycystic. The serum levels of T, LH and MDAwere significantly increased （P <0.05）, while the contents of E2, FSH and the activities of GSH-Px and SOD were significantly decreased （P <0.05）. The levels of MDA, StAR, cleaved caspase-3 and Bax proteins in ovarian tissue were significantly up-regulated （P <0.05）. GSH-Px and SOD activities and Bcl-2 protein levels were significantly down-regulated （P <0.05）. CONCLUSION Astragalosideeffectively balances the levels of sex hormone in PCOS rats and relieves the oxidative stress injury, the mechanism may be related to the inhibition of StAR expression. 相似文献
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YUE Ji-ping WANG Jin ZHANG Wen-ting ZHANG Zhi-nan JIN Wen-wen JIAO Xiang-ying 《园艺学报》2020,36(3):444-450
AIM: To investigate the effects of angiotensin Ⅱ type 1 receptor autoantibody (AT1-AA) on oxidative stress, autophagy and apoptosis in H9c2 cells, and to analyze the possible mechanism. METHODS: The rat H9c2 cells were cultured in vitro . The effect of AT1-AA at different concentrations for different time on the cell viability was measured by CCK-8 assay. Upon the optimum concentration (10-5 mol/L) and time point (24 h) determined in this stu-dy, the experssion levels of autophagy- and apoptosis-related proteins were detected by Western blot, and the levels of glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and malondialdehyde (MDA) were examined by oxidative stress kits. RESULTS: AT1-AA decreased cell viability in a concentration- and time-dependent manner, promoted apoptosis, and up-regulated the levels of autophagy and oxidative stress (P <0.05). The apoptosis of H9c2 cells induced by AT1-AA was decreased after pretreatment with autophagy inhibitor 3-methyladenine (P <0.05). The levels of autophagy and apoptosis in the H9c2 cells pretreated with α-lipoic acid were decreased (P <0.05). Pretreatment with angiotensin Ⅱtype 1 receptor inhibitor telmisartan inhibited oxidative stress, and significantly decreased the levels of autophagy and apoptosis induced by AT1-AA in the H9c2 cells (P <0.05). CONCLUSION: AT1-AA induces autophagy and apoptosis of H9c2 cells through oxidative stress. 相似文献
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AIM To investigate the mechanism of long noncoding RNA （lncRNA） FEZF1-AS1 regulating microRNA-363-3p （miR-363-3p） on the viability and apoptosis of lipopolysaocharide （LPS）-induced vascular endothelial cells. METHODS Human umbilical vein endothelial cells （HUVECs） were cultured in vitro . pcDNA-NC, pcDNA-FEZF1-AS1, anti-miR-NC, anti-miR-363-3p, miR-NC and miR-363-3p mimics were transfected into the HUVECs and LPS stimulation was applied for 24 h. RT-qPCR was used to detect the expression of FEZF1-AS1 and miR-363-3p. The cell viability was measured by MTT assay. The apoptotic rate was analyzed by flow cytometry. The dual-luciferase reporter experiment was used to verify the targeted regulation of FEZF1-AS1 and miR-363-3p. Western blot was used to determined the expression of cyclin D1, Ki67 and cleaved caspase-3. RESULTS Compared with control group, the expression level of FEZF1-AS1 in LPS group was significantly reduced （P <0.05）, and the expression level of miR-363-3p was significantly increased （P <0.05）. Compared with pcDNA-NC+LPS group, the cell viability in pcDNA-FEZF1-AS1+LPS group was significantly increased （P <0.05）, the apoptotic rate was significantly reduced （P <0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P <0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P <0.05）. Compared with anti-miR-NC+LPS group, the cell viability in anti-miR-363-3p+LPS group was significantly increased （P <0.05）, the apoptotic rate was significantly reduced （P <0.05）, the protein levels of cyclin D1 and Ki67 were significantly increased （P <0.05）, and the protein level of cleaved caspase-3 was significantly reduced （P <0.05）. Dual-luciferase reporter experiment confirmed that FEZF1-AS1 targeted miR-363-3p. Compared with miR-NC+pcDNA-FEZF1-AS1+LPS group, the cell viability in miR-363-3p+pcDNA-FEZF1-AS1+LPS group was significantly reduced （P <0.05）, the apoptotic rate was significantly increased （P <0.05）, the protein levels of cyclin D1 and Ki67 were significantly reduced （P <0.05）, and the protein level of cleaved caspase-3 was significantly increased （P <0.05）. CONCLUSION Over-expression of FEZF1-AS1 promotes the viability and inhibits apoptosis of LPS induced vascular endothelial cells by inhibiting the expression of miR-363-3p. 相似文献
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AIM To observe the effect of Chaihu-Shugan decoction (CHSGD) on atherosclerosis in spontaneously hypertensive rats (SHR) and its possible mechanism. METHODS The male SHR (n =50) were randomly divided into model group (gavage of normal saline), compound kendir leaves (CKL) group (gavage of 0.5 g/kg CKL), and low-, medium- and high-dose CHSGD (CHSGD-L, CHSGD-M and CHSGD-H) groups (gavage of 2.5, 5 and 10 g/kg CHSGD, respectively), and another 10 male Wistar rats of the same origin were selected as normal control （NC) group (gavage of normal saline). The blood pressure was measured by intelligent noninvasive sphygmomanometer. The levels of blood lipids were measured by automatic biochemical analyzer. The expression of oxidative stress-related indexes, nitric oxide (NO), malondialdehyde (MDA) and superoxide dismutase (SOD), were detected by colorimetry. HE staining was used to detect the degree of atherosclerosis, and Western blot was used to detect the expression of Rho-associated kinase (ROCK)/c-Jun N-terminal kinase (JNK) signaling pathway-related proteins, RhoA, ROCK1 and JNK. RESULTS After 4 weeks of treatment, compared with NC group, the blood pressure, the serum levels of triglyceride (TG), total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C) and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in model group were significantly increased (P <0.05), and the serum levels of high-density lipoprotein cholesterol, NO and SOD were significantly decreased (P <0.05). HE staining showed that the diameter of aortas in the rats was thickened, a large number of foam cells were formed under the endothelium, and the proliferation of smooth muscle cells was observed. Compared with model group, the blood pressure, the serum levels of TG, TC, LDL-C and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in CKL, CHSGD-L, CHSGD-M and CHSGD-H groups were significantly decreased (P <0.05), and the serum levels of NO and SOD were significantly increased (P <0.05). HE staining showed that the structure of each layer of rat aortas gradually returned to normal, the vascular cells were in good order, and the inflammatory cell infiltration was slight. Compared with CKL group, the blood pressure, the serum levels of TG, TC, LDL-C and MDA, and the protein expression of RhoA, ROCK1 and JNK in aortic tissues of the rats in CHSGD-L and CHSGD-M groups were significantly increased (P <0.05), and the serum levels of NO and SOD were significantly decreased (P <0.05). No significant difference of the above indexes between CHSGD-H group and CKL group was observed (P >0.05). CONCLUSION Chaihu-Shugan decoction may attenuate the oxidative stress response via inhibition of ROCK/JNK signaling pathway, thus alleviating the symptoms of atherosclerosis in SHR. 相似文献
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Role and potential mechanism of fecal microbiota transplantation in treatment of chronic hepatitis B
WEI Qi YANG Jing-nan HE Xue-liang HE Qiao-ling SI Hui-fang HU Hong BAI Chun-yang WANG Hui-chao LIN Xu-hong 《园艺学报》2000,36(10):1833-1843
AIM To investigate the effect of fecal microbiota transplantation （FMT） on the treatment of chronic hepatitis B （CHB） and the potential mechanism. METHODS Fifty C57BL/6J mice （6~8 weeks old） were divided into 5 groups： control group, CHB group, entecavir （ETV） group, comprehensive treatment （ETV+FMT, EFMT） group, and blocker （TAK-242+ETV+FMT, EFMT-TAK） group. The mice in each group were given corresponding treatment. The general condition of the mice was observed daily, and fecal specimens were kept every 10 d. The mice were sacrificed after 12 weeks, and the liver tissues and blood samples were collected. HE staining was used for histological scoring. Serum hepatitis B surface antigen （HBsAg） and interleukin-18 （IL-18） levels were measured by ELISA. Toll-like receptor 4 （TLR4） expression was detected by flow cytometry. Intestinal flora diversity was analyzed by high-throughput sequencing. RESULTS （1） Compared with control group, the body weight of the mice in CHB group was significantly reduced （P <0.05）. The body weight loss of the mice in ETV group, EFMT group and EFMT-TAK group was reversed to some extent as compared with CHB group （P <0.05）. （2） The histological score of the mice in CHB group was significantly higher than that in control group （P <0.05）. The score in ETV group was lower than that in CHB group （P <0.05）. The scores in EFMT group and EFMT-TAK group were lower than that in ETV group （P <0.05）, and that in EFMT-TAK group had a further downward trend compared with EFMT group （P <0.05）. （3） Compared with control group, the serum level of HBsAg in the CHB mice was significantly increased （P <0.05） and decreased after ETV treatment （P <0.05）. The HBsAg level in both EFMT group and EFMT-TAK group was significantly lower than that in ETV group （P <0.05）. （4） The IL-18 level in CHB group was significantly higher than that in control group （P <0.05）. After ETV treatment, the IL-18 level was decreased （P <0.05）, and that in both EFMT group and EFMT-TAK group was decreased more than that in ETV group （P <0.05）. （5） TLR4 expression in CHB group was higher than that in control group （P <0.05）, that in ETV group was lower than CHB group （P <0.05）, and that in EFMT group was further decreased （P <0.05）. （6） The heat map analysis at the class level showed that the abundances of Gammaproteobacteria , Deltaproteobacteria and Negativicutes in CHB group were significantly higher than those in control group, and those of Deltaproteobacteria and Negativicutes in EFMT group were close to those in control group. The heat map analysis at the family level indicated that the abundances of Burkholderiaceae , Desulfovibrionaceae and Veillonellaceae in CHB group were significantly higher than those in control group, while those in ETV group and EFMT group gradually approached normal levels. The α diversity index in CHB group was significantly decreased, while the diversity in ETV group was increased, that in EFMT group was further increased, and that in EFMT-TAK group was the highest. CONCLUSION FMT plays an active role in the treatment of CHB. The mechanism may be related to reducing the level of IL-18 and improving the structure and diversity of intestinal flora. The TLR4 signaling pathway is involved. 相似文献
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AIM To investigate the protective effects of gabexate mesilate （GM） on blood-brain barrier （BBB） permeability in rat model with cerebral ischemia-reperfusion （I/R）. METHODS Adult male SD rats （n =180） were randomly divided into sham group, I/R group, nimodipine （NMP; 2 mg·kg-1·d-1） group and GM （5, 10 and 20 mg·kg-1·d-1） groups （n =30 in each group）. The rat model of cerebral I/R was established by blocking the middle cerebral artery with thread plug for 2 h. Ten min before modeling, the drugs were given intraperitoneally. The nerve function was detected by Longa scoring method. The permeability of BBB was measured by Evans blue permeation method, and the brain water content was measured by dry-wet weight method. The activity of superoxide dismutase （SOD） and glutathione peroxidase （GSH-Px）, and the content of malondialdehyde （MDA） in brain tissue were determined by biochemical analysis. The content of tumor necrosis factor-α （TNF-α）, interleukin-1β （IL-1β） and IL-6 was measured by ELISA. The mRNA expression of matrix metalloproteinase-2 （MMP-2）, MMP-9 and nuclear factor-κB （NF-κB） was detected by RT-PCR. The protein levels of MMP-2, MMP-9 and NF-κB were determined by Western blot. RESULTS Compared with I/R group, the Longa score, permeability of Evans blue and brain water content of the rats in GM （10 and 20 mg·kg-1·d-1） and NMP （2 mg·kg-1·d-1） groups were decreased. The activity of SOD and GSH-Px was increased, while the content of MDA was decreased. The content of TNF-α, IL-1β and IL-6 was decreased, and the mRNA and protein expression levels of MMP-2, MMP-9 and NF-κB were significantly down-regulated. Compared with NMP （2 mg·kg-1·d-1） group, the Longa score and permeability of Evans blue were decreased in GM （20 mg·kg-1·d-1） group, the activity of SOD was increased, and the content of MDA and TNF-α was decreased. The mRNA and protein expression levels of MMP-2, MMP-9 and NF-κB were down-regulated. All of the differences were significant （P <0.05 or P <0.01）. CONCLUSION GM has protective effect on BBB in the rats with cerebral I/R. Its mechanism may be related to inhibition of oxidative stress and inflammation, and down-regulation of MMP-2, MMP-9 and NF-κB expression. 相似文献
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JIN Bei-fang LU Qin-zhen ZHANG Yan CUI Ya-lan QIANG Zheng LIAO Man-xi TAN Hui-yuan LIU Fang 《园艺学报》2000,36(9):1625-1630
AIM To explore the effects of oxidative stress and inflammatory response on kidney injury induced by hyperthyroidism in mice. METHODS Forty male Kunming mice were randomly divided into control group （n =20） and L-thyroxine （T4） group （n =20）. The mice in T4 group were intraperitoneally injected with T4 diluent at a dose of 1 mg/kg to induce hyperthyroidism, and those in control group were injected with normal saline of the same volume. After 7 weeks, the mice were weighed and dissected, the kidneys were removed and weighed, and the length of tibia was also measured. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the kidney tissues were detected. The pathological changes of the kidney tissues were observed by HE staining. The levels of 4-hydroxynonenal （4-HNE）-modified proteins, interleukin-1 receptor-associated kinase 1 （IRAK1） and tumor necrosis factor receptor-related factor 6 （TRAF6） were determined by Western blot and immunohistochemistry. RESULTS Compared with control group, the body weight of the mice was decreased, while the kidney size and weight were increased significantly in T4 group. In addition, the ratios of kidney weight/body weight and kidney weight/tibia length were also increased （P <0.05）. In T4 group, the renal tubules were enlarged, and the epithelial cells of renal tubules were swollen and exfoliated, with vacuolar degeneration. Furthermore, reduced SOD activity, and increased MDA content and 4-HNE-modified proteins were found in T4 group, all of which were related to oxidative stress （P <0.05）. The levels of inflammation-related proteins IRAK1 and TRAF6 were significantly increased in T4 group （P <0.05）. CONCLUSION Excessive T4 may lead to kidney hypertrophy and injury in mice, and the mechanism may be related to oxidative stress and inflammatory response. 相似文献
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AIM To explore the inhibitory effect of metformin （MET） on nerve injury in rats with stroke and its mechanism. METHODS SD rats were randomly divided into sham group （n =15）, model group （n =30）, MET group （n =30）, MET+agomir-NC group （n =30） and MET+agomir group （n =30）. The modified Puisinelli four-vessel occlusion method was used to prepare the model of global ischemic stroke, while the blood vessels in sham rats were isolated without clamping the common artery. One week before modeling, the rats in MET group, MET+agomir-NC group and MET+agomir group were given intraperitoneal injection of 100 mg·kg-1·d-1 MET, 100 mg·kg-1·d-1 MET+40 nmol/d agomir-NC, 100 mg·kg-1·d-1 MET+40 nmol/d miR-29c agomir, respectively, and the rats in sham group and model group were given intraperitoneal injection of the same amount of normal saline. Each treatment in the above groups was given once a day, 0.2 mL each time, for 7 consecutive days. The neurological deficit scores were measured 24, 48 and 72 h after operation. HE staining was used to observe the morphological changes of the hippocampus, and the living neurons were counted. RT-qPCR was used to detect the expression level of miR-29c, and the mRNA levels of silent information regulator 1 （SIRT1） and peroxisome proliferator-activated receptor γ coactivator 1α （PGC-1α） in hippocampus. The protein expression levels of SIRT1 and PGC-1α were determined by Western blot. RESULTS At the same time point, compared with model group, the neurological deficit score in MET group was significantly decreased, and the survival rate of the neurons was significantly increased （P <0.05）. Compared with MET+agomir-NC group, the neurological deficit score in MET+agomir group was increased, and the survival rate of the neurons was significantly decreased （P <0.05）. With the prolongation of time, except for sham group, the neurological deficit score was increased and the survival rate of the neurons was decreased. At 72 h after operation, compared with sham group, the expression of miR-29c in hippocampus of model group was significantly increased, and the mRNA and protein expression levels of SIRT1 and PGC-1α were significantly decreased （P <0.05）. Compared with model group, the expression of miR-29c in hippocampus of MET group was significantly decreased, and the expression of SIRT1 and PGC-1α at mRNA and protein levels was significantly increased （P < 0.05）. Compared with MET+agomir-NC group, the expression of miR-29c in hippocampus of MET+agomir group was significantly increased, and the mRNA and protein expression of SIRT1 and PGC-1α was significantly decreased （P <0.05）. CONCLUSIONS MET alleviates nerve injury in stroke rats, which may be related to down-regulation of miR-29c and promotion of SIRT1/PGC-1α signaling pathway activation. 相似文献
15.
AIM To investigate the effectof flax lignan/secoisolariciresinol diglucoside （SDG） on the inflammatory damage of kidney induced by chronic intermittent hypoxia （CIH）. METHODS C57BL/6N mice were divided into normal （control） group, model （CIH） group and treatment （SDG） group. The changes of the body weight was recorded. Hematoxylin-eosin （HE） staining was used to observe the morphological alterations in the renal tissues. The levels of serum creatinine and blood urea nitrogen were measured by a biochemical analyzer. Hydroxylamine and thiobarbituric acid methods were used to detect the activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） in the renal tissues. The protein levels of thioredoxin-interacting protein （TXNIP） and nucleotide-binding oligomerization domain-like receptor protein 3 （NLRP3） were detected by immunohistochemical staining, while those of tumor necrosis factor-α （TNF-α）, interleukin-6 （IL-6） and IL-1β were measured by ELISA. The protein levels of TXNIP, NLRP3, apoptosis-associated speck-like protein containing a CARD （ASC）, caspase-1, IL-1β and IL-18 in the renal tissues were also determined by Western blot. RESULTS No significant difference in the body weight and kidney index among the 3 groups was observed （P >0.05）. HE staining showed the swollen epithelial cells of renal tubules with vesicular degeneration, and irregular glomerular morphological change in CIH group, while SDG treatment attenuated the above changes. Compared with control group, the levels of serum creatinine, TNF-α, IL-6 and IL-1β were significantly increased in CIH group （P <0.05）. The significantly increased expression levels of NLRP3 and TXNIP in the cytoplasm of renal tubular epithelial cells in CIH group were detected by immunohistochemical staining. Compared with control group, the activity of SOD was decreased, the content of MDA was increased in CIH group, and the protein expression levels of TXNIP, NLRP3, ASC, caspase-1, IL-1β and IL-18 were up-regulated and then decreased after SDG treatment （P <0.05）. CONCLUSION SDG attenuates the renal inflammatory damage of the mice induced by CIH, and its mechanism may be associated with the inhibition of oxidative stress and activation of NLRP3 inflammasome. 相似文献
16.
AIM To investigate the effect of forsythiaside A (FA) on immune function in rats with ulcerative colitis and its related mechanism. METHODS Healthy SD rats were randomly divided into 5 groups: control group (no treatment, normal feeding), model group (establishment of rat ulcerative colitis model), and low, medium and high doses of FA groups (treatment of the model rats with FA at 5 mg/kg, 20 mg/kg and 80 mg/kg, respectively). The malondialdehyde (MDA) content and superoxide dismutase (SOD) activity in rat colon tissues were measured by colorimetry, and the serum levels of tumor necrosis factor-α (TNF-α), interleukin-2 (IL-2) and IL-4 were detected by ELISA. The spleen index and thymus index, the percentages of CD3+, CD4+ and CD8+ T-lymphocytes in peripheral blood mononuclear cells （PBMC）, the serum IgA and IgG levels, and the serum complement C3 and C4 levels were also determined. RESULTS The colon tissues of the rats in model group showed obvious inflammation and ulceration, indicating that the animal model was successfully established. Compared with model group, the colonic inflammation and ulceration were significantly attenuated in FA groups, among which the high dose had the best effect. Compared with control group, the spleen index and thymus index of the rars in model group were decreased (P <0.05), MDA content in colon tissues was increased (P <0.05), and SOD activity in colon tissues was decreased (P <0.05). The levels of CD3+, CD4+, CD8+ and CD4+/CD8+ T-lymphocytes in PBMC, and the serum levels of C3, C4 and IL-4 were decreased (P <0.05), while the serum levels of IgA, IgG, TNF-α, and IL-2 were increased in model group as compared with control group. Furthermore, the spleen index and thymus index of the rats in FA groups were increased (P <0.05), the MDA content in the colon tissues was decreased (P <0.05), and the SOD activity in the colon tissues was increased (P <0.05). The levels of CD3+, CD4+, CD8+ and CD4+/CD8+ T-lymphocytes in PBMC, and the serum levels of C3, C4 and IL-4 were increased (P <0.05), while serum IgA, IgG, TNF-α and IL-2 levels were decreased in FA groups as compared with model group (P <0.05). CONCLUSION Forsythiaside A effectively attenuates the colonic lesions in rats with ulcerative colitis, and its mechanism may be related to reinforcement of oxygen free radical scavenging power, alleviation of inflammatory response, and enhancement of immune function. 相似文献
17.
AIM To investigate the effects of geniposide （Gen） on Toll like receptor 4/nuclear factor-κB （TLR4/NF-κB） signaling pathway and cognitive dysfunction in sleep deprived rats. METHODS Wistar rats （n =120） were randomly divided into normal control （NC） group, model （M） group, low-dose （5 g·kg-1·d-1） Gen （Gen-L） group, medium-dose （10 g·kg-1·d-1） Gen （Gen-M） group, high-dose （20 g·kg-1·d-1） Gen （Gen-H） group and Gen-H+LPS （0.4 mg·kg-1·d-1, tail vein injection） group. After 7 days of intervention, the sleep deprivation model of rats in M group, Gen-L, Gen-M, Gen-H and Gen-H+LPS group was established by improved small platform water environment. The escape latency of Morris water maze experiment and the behavior correct rate of Y maze experiment were measured. The serum levels of S100B and neuron-specific enolase （NSE）, and the levels of interleukin-1β （IL-1β）, IL-6 and tumor necrosis factor-α （TNF-α） in hippocampus were detected by ELISA. The mRNA levels of TLR4 and NF-κB p65 were detected by RT-qPCR, and the protein levels of TLR4 and NF-κB p65 were determined by Western blot. RESULTS Compared with NC group, the escape latency, the serum levels of S100B and NSE, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the mRNA and protein expression of TLR4 and NF-κB p65 were increased significantly in M group （P <0.01）, and the behavior correct rate was decreased significantly （P <0.01）. Compared with M group, the escape latency, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were decreased significantly in Gen-L, Gen-M and Gen-H groups （P <0.01）, and the behavior correct rate was increased in turn （P <0.01）. Compared with Gen-H group, the escape latency, the serum levels of S100B and NSE, the hippocampal levels of IL-1β, IL-6 and TNF-α, and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were increased significantly in Gen-H+LPS group （P <0.01）, and the behavior correct rate was decreased significantly （P <0.01）. CONCLUSION Geniposide may inhibit the TLR4/NF-κB p65 signaling pathway to effectively improve cognitive function in sleep-deprived rats and reduce hippocampus inflammation. 相似文献
18.
Destruction of autophagy marker LC3 rhythm is involved in β1-AA-induced H9c2 rat cardiomyocyte death
JIA Wei-wei NING Na SUN Cong LI Peng-jia LU Jie-bei ZHANG Sheng YUAN Yuan WANG Li WANG Xiao-hui 《园艺学报》2021,37(1):10-17
AIM To investigate the effect of β1-adrenergic receptor autoantibodies （β1-AA） on the rhythm of autophagy marker microtubule-associated protein 1 light chain 3 （LC3）, and the underlying mechanism of cardiomyocyte death. METHODS The test materials were Sprague-Dawley （SD） rats and H9c2 rat cardiomyocytes. The SD rats were randomly divided into immunization group and control group with 6 rats in each group. The H9c2 cells were randomly divided into control group, β1-AA group, lentivirus （LV）-NC group, and LV-shPer2 group （n =6）. Affinity chromatography was used for purification of β1-AA from rat serum. CCK-8 assay was used to observe the viability of cardiomyocytes treated with β1-AA for 24 h. The cells were synchronized by dexamethasone and then treated with β1-AA. The mRNA and protein levels of LC3 at different time points were determined by real-time PCR and Western blot, respectively. The Per2 protein level at different time points was also determined by by Western blot. JTK_CYCLE algorithm was used to estimate the circadian rhythm parameters. After destruction of LC3 circadian rhythm via LV-shPer2, CCK-8 assay was used to measure the viability of H9c2 cells. RESULTS High level of β1-AA in rat serum was found after active immunization compared with control group （P <0.05）. The viability of H9c2 cells in β1-AA group was significantly lower than that in control group （P <0.05）. The LC3 and Per2 rhythms were both disrupted in H9c2 cells induced by β1-AA （JTK_CYCLE P <0.05）. After LV-shPer2 infection, the LC3 rhythm was disrupted （JTK_CYCLE P <0.05） and the cell viability was reduced （P <0.05）. CONCLUSION β1-AA may induce the destruction of autophagy marker LC3 rhythm in rat cardiomyocytes and then promote cell death. 相似文献
19.