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1.
AIM To investigate the effect of mangiferin on hypoxia/reoxygenation (H/R)-induced injury of human myocardial cells and its mechanism. METHODS Human myocardial AC16 cells were divided into normal group, H/R group and H/R + mangiferin (50, 100 and 200 μmol/L) treatment groups. The mRNA and protein expression levels of Kelch-like epichlorohydrin-associated protein-1 (Keap-1), Bax, Bcl-2, caspase-3, caspase-9 and superoxide dismutase 2 (SOD2) were detected by RT-qPCR and Western blot, respectively. The protein expression of nuclear factor E2-related factor 2 (Nrf-2) in nucleus was determined by Western blot. The expression of microRNA-432-3p (miR-432-3p) was detected by RT-qPCR. The generation of reactive oxygen speciess (ROS) in the cells was measured by DCFH-DA probing. The cell viability was measured by CCK-8 assay. Apoptosis was analyzed by flow cytometry. RESULTS No significant difference in the expression of miR-432-3p and Keap-1 between normal group and H/R group was observed. Compared with normal group, the nuclear translocation of Nrf-2, the ROS level, and the mRNA and protein expression of Bax, caspase-3 and caspase-9 were significantly increased in H/R group （P <0.05）. The mRNA and protein expression of SOD2 and Bcl-2, and the cell viability significantly decreased in H/R group compared with normal group, while the apoptosis was increased significantly （P <0.05）. Treatment with mangiferin resulted in an increase in the miR-432-3p expression and a decrease in the ROS level, and the expression of Keap-1, Bax, caspase-3 and caspase-9 was also inhibited as compared with H/R group （P <0.05）. The Nrf-2 nuclear translocation, and the protein levels of SOD2 and Bcl-2 in mangiferin treatment groups were significantly increased as compared with H/R group （P <0.05）. The cell viability was increased significantly, and the apoptosis was decreased significantly in mangiferin treatment groups as compared with H/R group （P <0.05）. The effects of mangiferin in middle- and high-dose groups were better than those in low-dose group, and no significant difference between middle- and high-dose groups was found. CONCLUSION Mangiferin inhibits the decrease in myocardial cell viability and the apoptosis induced by H/R injury. The mechanism may be related to the up-regulation of Nrf-2 antioxidant stress effect via enhancing the expression of miR-432-3p. 相似文献
2.
ZHAO Yan-jiao YAN Yuan-yuan LI Dan LUO Xue-lan YANG Peng ZHOU Fu-long YANG Rui-xia TANG Shuang-yi OU He-sheng 《园艺学报》2000,36(10):1745-1753
AIM To investigate the effect of 27nt-miRNA （27nt-miR） on apoptosis of human umbilical vein endothelial cells （HUVECs） induced by oxidized low-density lipoprotein （Ox-LDL） and its underlying mechanism. METHODS HUVECs were cultured in vitro and grouped as below： normal control group, Ox-LDL group, 27nt-miR+Ox-LDL group, anti-27nt-miR+Ox-LDL group and negative control+Ox-LDL group. The cells in Ox-LDL group were treated with Ox-LDL at 40 mg/L for 48 h, while those in normal control group were untreated but cultured normally. The cells in 27nt-miR+Ox-LDL group, anti-27nt-miR+Ox-LDL group and negative control+Ox-LDL group were transfected with their corresponding lentiviral vectors under the same procedure, followed by treatment with Ox-LDL at 40 mg/L for 48 h to induce apoptosis. The cell viability was measured by CCK-8 assay. The migration capacity was detected by scratch assay. The caspase-3 activity was measured by caspase-3 activity assay kit. The apoptotic rate was analyzed by Hoechst 33258 and flow cytometry. The mRNA and protein expression levels of Bcl-2, Bax and caspase-3 were determined by RT-qPCR and Western blot. RESUITS： Compared with negative control+Ox-LDL group, the cell viability and migration ability were significantly decreased by over-expression of 27nt-miR in the HUVECs （P <0.05）, while the activity of caspase-3 and apoptosis induced by Ox-LDL were significantly increased （P <0.05）. Furthermore, the mRNA and protein expression levels of Bax and caspase-3 were significantly up-regulated （P <0.05）, and the mRNA and protein expression level of Bcl-2 was down-regulated in 27nt-miR+Ox-LDL group （P <0.05）. Meanwhile, all the above indexes showed an opposite tendency in anti-27nt-miR+Ox-LDL group. CONCLUSION 27nt-miR promotes Ox-LDL-induced apoptosis and inhibits the viability and migration of HUVECs in vitro , possibly through regulating the expression of apoptotic/anti-apoptotic proteins such as Bax,caspase-3 and Bcl-2. 相似文献
3.
AIM To investigate the expression of baculoviral inhibitor of apoptosis protein repeat-containing protein 5 （BIRC5） in gastric cancer tissue and its relationship with prognosis of gastric cancer patients, and to explore the effect of BIRC5 knock-down on the viability and apoptosis of gastric cancer cells. METHODS The expression of BIRC5 was detected by immunohistochemistry in 67 cases of gastric cancer tissues and paracancerous tissues for analyzing the relationships with clinicopathological characteristics. The mRNA and protein expression levels of BIRC5 in gastric carcinoma cell lines （AGS, MKN-1 and MGC-803） and normal gastric epithelial cell line GES-1 were detected by RT-qPCR and Western blot. The AGS cells were divided into blank group （no treatment）, Ctr-sh group （blank plasmid transfection） and BIRC5-sh group （BIRC5-shRNA plasmid transfection）. The interference efficiency of BIRC5-shRNA was evaluated by Western blot. The cell viability was measured by MTT assay, the apoptosis was analyzed by flow cytometry, and the levels of apoptosis-related proteins cleaved caspase-3, Bax and Bcl-2 were determined by Western blot. RESULTS BIRC5 was mainly expressed in cytoplasm, and the positive expression rate of BIRC5 in the gastric cancer tissues was higher than that in the adjacent tissues （P <0.01）. The positive rates of BIRC5 in the gastric cancer patients at TNM Ⅲ~Ⅳ stages and with lymph node metastasis were higher than those in the patients at TNM Ⅰ~Ⅱ stages and without lymph node metastasis, respectively （P <0.05）. The survival time of the patients with positive BIRC5 expression was shorter than that of the patients with negative BIRC5 expression （P =0.011 2）. The cell viability in BIRC5-sh group was lower than that in blank group and Ctr-sh group at time points of 48, 72 and 96 h. The apoptotic rate in BIRC5-sh group was increased compared with blank group and Ctr-sh group. The protein levels of cleaved caspase-3 and Bax in BIRC5-sh group were higher than those in blank group and Ctr-sh group, while the protein expression of Bcl-2 in BIRC5-sh group was lower than that in blank group and Ctr-sh group （P <0.05）. CONCLUSION High expression of BIRC5 in gastric cancer indicates poor prognosis. BIRC5 promotes the growth of gastric cancer cells and inhibits apoptosis. 相似文献
4.
LI Xiao-wen ZHOU Yue-han DENG Jian-zhi LUO Zhen-hua JIANG Hai-jian ZHANG Man-li QIN Chu-ling 《园艺学报》2020,36(6):977-984
AIM To explore the effect of andrographolide (AND) on the growth and apoptosis of acute lymphoblastic leukemia （ALL） cells. METHODS CCK-8 assay was used to assess the viability of human acute lymphoblastic leukemia CEM-C1 cells treated with AND for 12 h, 24 h and 48 h. The cell morphological changes were observed by Wright-Giemsa staining. The cell apoptosis was detected by flow cytometry with annexin V-FITC/propidium iodide (PI) staining, and the cell cycle was examined by flow cytometry with PI staining. The expression levels of apoptosis-related proteins were examined by Western blot. The mitochondrial membrane potential (MMP) of the cells was determined by JC-1 assay. RESULTS The results of CCK-8 assay indicated that AND inhibited the viability of CEM-C1 cells in a dose- and time-dependent manner. After administration of AND for 24 h, CEM-C1 cells shrank, the cytoplasm turned red and the cell numbers were significantly reduced. Incubation of AND for 24 h resulted in G2-phase arrest and apoptosis. Treatment with AND for 24 h increased the protein levels of cleaved caspase-3, cleaved caspase-7 and Bax, and down-regulated Bcl-2 in the CEM-C1 cells (P <0.05). The ratios of cleaved caspase-3/caspase-3, cleaved caspase-7/caspase-7 and Bax/Bcl-2 were elevated with the increase in the concentration of AND. Collapsed MMP in CEM-C1 cells was observed after AND administration for 24 h. Treatment with AND in vivo suppressed the growth of the xenograft tumor and increased the protein level of cleaved caspase-3. CONCLUSION Andrographolide exerts growth-inhibitory and apoptosis-inducing effects on ALL cells both in vitro and in vivo . 相似文献
5.
ATM: To explore the possibility that advanced glycation end products (AGEs) induces rat chondrocyte injury by modulating oxidative stress. METHODS: Primarily cultured rat chondrocytes were identified. The viability of the chondrocytes was measured by CCK-8 assay. The intracellular levels of reactive oxygen species (ROS) were detected by DCFH-DA staining. The number of apoptotic cells was determined by Hoechst 33342 nuclear staining and flow cytometry. RT-PCR was performed to measure the mRNA levels of Bax, Bcl-2, caspase-3, MMP3, MMP13 and COL2 in the chondrocytes. Western blotting was used to evaluate the protein levels of cleaved caspase-3, MMP3, MMP13 and COL2. RESULTS: Compared with control group, the intracellular levels of ROS in the chondrocytes treated with AGEs were significantly increased (P<0.05), and pretreatment with N-acetyl-L-cysteine (NAC) suppressed the formation of ROS (P<0.05). Besides, NAC inhibited AGEs-induced apoptosis of the chondrocytes, as indicated by reduceing the levels of Bax/Bcl-2 and caspase-3, decreased the expression of MMP3 and MMP13, and reduced the loss of COL2.CONCLUSION: AGEs induce chondrocyte injury by activating oxidative stress. 相似文献
6.
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
7.
HUANG Hua-kun YUAN Xiao-hui ZHANG Ping YU Ting-ting ZHANG Lu-lu YANG Chun-mei LUO Xiao-ji LUO Jin-yong 《园艺学报》2020,36(4):628-636
AIM To investigate the inhibitory effect of andrographolide （AG） on human osteosarcoma 143B cells and its underlying molecular mechanism. METHODS Osteosarcoma 143B cells were cultured in vitro and treated with AG at different concentrations (0~20 μmol/L), and the effect of AG on the proliferation of 143B cells was determined by crystal violet staining, MTT assay and colony formation assay. The wound-healing assay was performed to detect the migration ability of osteosarcoma 143B cells. Transwell assay was performed to analyze the invasive capacity of osteosarcoma 143B cells. The effect of AG on the apoptosis of osteosarcoma 143B cells was detected by Hoechst 33258 staining and flow cytometry. After treatment with of AG at different concentrations, the protein levels of the molecules related to proliferation, migration, invasion and apoptosis of osteosarcoma 143B cells were determined by Western blot. The expression of β-catenin and its related molecule c-Myc in the Wnt signaling pathway was analyzed by Western blot. RESULTS Compared with blank group, the proliferation, migration and invasion of osteosarcoma 143B cells in AG treatment group were significantly inhibited (P <0.05) in a concentration-dependent manner. The expression levels of invasion- and migration-related proteins matrix metalloproteinase-9 (MMP-9), vimentin and Snail were all down-regulated (P <0.05). AG also increased the expression of antiapoptotic protein Bcl-2, and the levels of apoptosis-related protein caspase-3 was decreased but cleaved caspase-3 was increased. At the same time, the expression levels of Wnt/β-catenin signaling pathway related proteins β-catenin and c-Myc were significantly decreased (P <0.05). CONCLUSION Andrographolide may inhibit the proliferation, migration, and invasion of osteosarcoma 143B cells and promote their apoptosis by inhibiting the activity of Wnt signaling pathway. 相似文献
8.
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
9.
WANG Yuan GAO Hong-wei FENG Gao-jie DAI Pei ZHANG Qin-feng BAI Rui QIN Wei-wei LI Hong GAO Fen 《园艺学报》2020,36(2):206-213
AIM: To compare the effects of high-density lipoprotein (HDL) from healthy subjects (HDLheathy) and HDL from the patients with coronary artery disease (HDLCAD) on the lipid deposition and apoptosis in mouse peritoneal macrophages. METHODS: HDL was isolated from healthy subjects, stable CAD patients (HDLSCAD) and acute myocar-dial infarction patients (HDLAMI). The accumulation of intracellular lipids was determined by oil red O staining. The apoptosis of macrophages was measured by fluorescence microscopy with annexin-V/PI staining. DCHF-DA, a redox-sensitive dye, was used to detect intracellular reactive oxygen species (ROS) levels. The protein expression of ATP-binding cassette transporter (ABC) A1, ABCG1, Bcl-2 and Bax was determined by Western blot analysis. RESULTS: Lipid deposition in the macrophages was increased significantly after oxidized low-density lipoprotein (ox-LDL) treatment, and the expression of ABCA1 and ABCG1 was up-regulated (P <0.05). Compared with ox-LDL treatment alone, HDLhealthy decreased lipid deposition in the macrophages and up-regulated the expression of ABCA1 and ABCG1 (P <0.05), while treatment with HDLSCAD or HDLAMI further decreased lipid deposition in the macrophages and down-regulated the expression of ABCA1 and ABCG1 (P <0.05). Compared with HDLSCAD treatment, lipid deposition in the macrophages was further increased after HDLAMI treatment, and the expression of ABCA1 and ABCG1 was down-regulated (P <0.05). HDLhealthy decreased the levels of intracellular ROS and apoptosis by increasing the level of antiapoptotic protein Bcl-2 and reducing the expression of proapoptotic protein Bax. In contrast, HDLSCAD and HDLAMI had opposite effects on the intracellular ROS, the cell apoptosis and the expression of apoptosis-related proteins Bcl-2 and Bax. CONCLUSION: HDLCAD promotes lipid accumulation in macrophages and induces macrophage apoptosis. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in CAD. 相似文献
10.
AIM To explore the effect of dasatinib on the viability, apoptosis and migration of human renal carcinoma cell lines 786-O and 769-P, as well as the molecular mechanism in vitro . METHODS 786-O cells and 769-P cells were treated with different concentrations （0~2 μmol/L） of dasatinib, and 0 μmol/L dasatinib was used as blank control group. MTT method was used to detect cell viability. Wound healing assay was used to detect the effect of dasatinib on migration. Hoechst 33258 staining was used to observe the effect of dasatinib on apoptosis. Flow cytometry was used to detect the effect of dasatinib on cell cycle. Western blot method was used to detected cell cycle- and apoptosis-related protein levels. RESULTS Dasatinib inhibited viability and migration of 786-O and 769-P cells, and the inhibitory effect of dasatinib increased with the concentration of dasatinib （P <0.05）. The IC50 values of dasatinib against 786-O and 769-P cell lines were （0.958 7±0.028 8） μmol/L and （0.784 3±0.066 0） μmol/L, respectively. After treatment with dasatinib for 24 h, the expression of pro-apoptotic proteins cleaved caspase-3 and cleaved caspase-9 increased significantly （P <0.01）, while the expression of cyclin D1 decreased （P <0.05）. The cycle-related pathway proteins p53 and p21 increased （P <0.05）, while the level of p-AKT was decreased （P <0.05）. CONCLUSION Dasatinib impaired the viability and migration ability of human renal carcinoma cell lines 786-O and 769-P by up-regulating p53 expression and down-regulating AKT phosphorylation. 相似文献
11.
QU Yi-ming SHAO Gao-hai ZHANG Ming-hua LI Bo ZHU Feng-chen HE Chao CAO Chun-feng ZHAO Bo 《园艺学报》2020,36(6):1089-1095
AIM To explore the effect of platelet-rich plasma (PRP) on rabbit osteoarthritis and its possible mechanism. METHODS The rabbits with knee osteoarthritis were prepared and then divided into model group, sodium hyaluronate (SH) group and PRP group, and another sham operation group was set up, with 6 rabbits in each group. The gross morphological changes of rabbit cartilage were observed. HE staining was used to evaluate the pathomorphological changes of the cartilage. TUNEL staining was used to detect the apoptosis of chondrocytes. The expression of nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)/interleukin-1β （IL-1β） signaling pathway-related molecules was observed by immunohistochemical staining, and the protein levels of caspase-3, Bcl-2 and Bax were determined by Western blot. Chondrocytes were isolated and processed according to grouping, and the NLRP3 and IL-1β levels of the cells were measured by ELISA. RESULTS Compared with sham operation group, Pelletier score, Mankin score, chondrocyte apoptotic rate, the positive protein expression rates of NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC), caspase-1 and IL-1β, and the protein levels of caspase-3 and Bax in model group were increased significantly (P <0.05), while the protein expression of Bcl-2 was decreased significantly (P <0.05). Compared with model group, Pelletier score, Mankin score, the apoptotic rate of chondrocytes, the positive protein expression rates of NLRP3, ASC, caspase-1 and IL-1β, and the protein levels of caspase-3 and Bax in SH group and PRP group were decreased significantly (P <0.05), while the protein expression of Bcl-2 was increased significantly (P <0.05). In PRP group, Pelletier score, Mankin score, the apoptotic rate of chondrocytes, the positive protein expression rates of NLRP3, ASC, caspase-1 and IL-1β, and the protein levels of caspase-3 and Bax were lower than those in SH group, while the protein expression of Bcl-2 was higher than that in SH group (P <0.05). Compared with control group, the expression of NL?RP3 and IL-1β in MCC950 (NLRP3 ihibitor) group were significantly reduced (P <0.05), the expression of NLRP3 in eucalyptol (IL-1β inhibitor) group was not significantly changed (P >0.05), and the expression of IL-1β was significantly reduced (P <0.05). CONCLUSION Platelet-rich plasma promotes the repair of cartilage in osteoarthritis rabbits, which has better effect than SH. The mechanism may be related to the inhibition of NLRP3/IL-1β pathway and the reduction of chondrocyte apoptosis. 相似文献
12.
WANG Li-min 《园艺学报》2015,31(9):1715-1719
AIM: To investigate the effect of Ginsenoside Rh2(Rh2) on the apoptosis of human osteosarcoma cell line MG-63.METHODS: The cell viability was determined by MTT assay. MG-63 cell apoptotic rate was examined by flow cytometry with Annexin V-PI double staining. The expression of Bcl-2, Bax, cytochrome C(Cyt C) and cleaved caspase-3 were measured by Western blot.RESULTS: Rh2 enhanced the apoptosis of MG-63 cells in a dose-dependent manner. Furthermore, after treatment with Rh2, the release of mitochondrial Cyt C and Bax expression were increased, while Bcl-2 and the ratio of Bcl-2/Bax were decreased as compared with control group(P<0.05). The protein level of cleaved caspase-3 was also increased(P<0.05).CONCLUSION: Ginsenoside Rh2 accelerates the apoptosis of MG-63 cells through mitochondria-dependent pathway, suggesting that Rh2 is a novel approach for the treatment of osteosarcoma. 相似文献
13.
AIM To investigate the effect of stanniocalcin-1 （STC-1） on the proliferation and apoptosis of gastric cancer AGS cells and the role of Bcl-2 in these processes. METHODS The AGS cells were transfected with the plasmids for STC -1 knockdown or over-expression. The cell proliferation was measured by MTT assay and colony formation assay. The migration ability was detected by scratch assay. Apoptosis was analyzed by Hoechst 33342 staining and flow cytometry with annexin V-FITC/PI double staining. The protein expression of Bcl-2, survivin, caspase-3 and cleared caspase-3 was determined by Western blot. The mRNA expression levels of STC-1 and Bcl-2 in 20 cases of clinical gastric cancer tissues and adjacent tissues were detected by RT-qPCR, and the correlation between them was analyzed by Pearson method. RESULTS After over-expression of STC-1, the proliferation and migration abilities of the AGS cells were increased, the expression of Bcl-2 and survivin was increased, while the expression of caspase-3 and cleared caspase-3 was decreased （P <0.05）. After knockdown of STC -1 , the proliferation and migration abilities of the AGS cells were decreased, the expression of Bcl-2 and survivin was decreased, while the expression of caspase-3 and cleared caspase-3 was increased （P <0.05）. The mRNA expression levels of STC-1 and Bcl-2 in the gastric cancer tissues were higher than those in the adjacent tissues. Pearson correlation analysis showed that there was a positive correlation between STC-1 and Bcl-2 mRNA expression in the cancer tissues （r =0.308, P =0.011）. CONCLUSION STC-1 may regulate the biological function of gastric cancer cells by altering the expression level of Bcl-2. 相似文献
14.
AIM To investigate the effect of prostaglandin E1 (PGE1) on heart after myocardial infarction (MI) in rats and its related molecular mechanism. METHODS Fifty male SD rats were divided into sham group, model group and model+PGE1 group. The MI rat model was established by ligation of left anterior descending coronary artery. Cardiac function in the rats was detected by echocardiogaphy. The myocardial histomorphologic changes were evaluated by HE and Masson staining. The MI area was measured by TTC staining. The cardiomyocyte death was detected by TUNEL staining. The protein levels of endoplasmic reticulum stress (ERS)-related factors glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP) and caspase-12, and apoptosis-related factors Bcl-2, Bax and cleaved caspase-3 were determined by immunofluorescence staining and Western blot. RESULTS Compared with sham group, the cardiac function in model group was decreased, with significant myocardial pathological changes. The MI area was enlarged, and the death of cardiomyocytes was promoted. The protein levels of GRP78, CHOP, caspase-12, Bax and cleaved caspase-3 in the myocardial tissues were significantly increased, while Bcl-2 was decreased (P <0.01). Compared with model group, the cardiac function in model+PGE1 group was significantly improved, and the myocardial pathological damage was significantlty attenuated. The MI area and myocardial cell death were significantly reduced. The protein levels of GRP78, CHOP, caspase-12, Bax and cleaved caspase-3 in the myocardial tissues were significantly decreased, while Bcl-2 was increased (P <0.01). CONCLUSION PGE1 reduces collagen deposition and inflammation, and improves cardiac function by reducing ERS level, thus protecting cardiomyocytes from MI damage. 相似文献
15.
AIM To study the effects of extracts of Herba Taxilli (Sangjisheng, SJS) on the viability and apoptosis of osteoarthritic chondrocytes and the underlying mechanism. METHODS Human primary osteoarticular chondrocytes (RPOC) were divided into control group, interleukin-1β (IL-1β) group, IL-1β+low-dose extracts of SJS (SJS-L) group, IL-1β+medium-dose extracts of SJS (SJS-M) group, IL-1β+high-dose extracts of SJS (SJS-H) group, IL-1β+anti-miR-NC group, IL-1β+anti-miR-375 group, IL-1β+SJS-H+miR-NC group, IL-1β+SJS-H+miR-375 group. The cell viability was measured by MTT assay, apoptosis was analyzed by flow cytometry, miR-375 expression was detected by qPCR, and the protein levels of cyclin D1, P21, Bcl-2, Bax and caspase-3 were determined by Western blot. RESULTS Compared with control group, the viability of RPOC at 24 h, 48 h and 72 h and the protein expression levels of cyclin D1 and Bcl-2 were significantly decreased (P <0.05), the protein levels of P21, Bax and caspase-3, the apoptotic rate and the expression level of miR-375 were remarkably increased in IL-1β group(P <0.05). Compared with IL-1β group, the cell viability at 24 h, 48 h and 72 h and the protein expression of cyclin D1 in the RPOC were greatly increased (P <0.05), while the expression of P21 was significantly decreased in IL-1β+SJS-M group and IL-1β+SJS-H group(P <0.05).The apoptotic rate, Bax, caspase-3 protein and miR-375 expression were obviously decreased (P <0.05), and Bcl-2 protein level was significantly increased in IL-1β+SJS-H group compared with IL-1β group(P <0.05). Compared with IL-1β+anti-miR-NC group, the expression of miR-375, the protein levels of P21, Bax, caspase-3 and the apoptotic rate in the RPOC of IL-1β+anti-miR-375 group were markedly decreased (P <0.05), while the cell viability at 24 h, 48 h and 72 h and the protein levels of cyclin D1 and Bcl-2 were significantly increased (P <0.05). Over-expression of miR-375 reversed the effects of extracts of SJS on the viability and apoptosis of RPOC with IL-1β stimulation. CONCLUSION The extracts of Herba Taxilli promotes the viability and inhibits apoptosis of RPOC treated with IL-1β, which is related to the regulation of miR-375 expression. 相似文献
16.
FENG Juan HOU Juan-ni FENG Jian TANG Ming-yang SONG Zhi-ping CHEN Sha PEI Hai-feng YANG Yong-jian 《园艺学报》2020,36(3):401-407
AIM: To investigate the effects of CR6-interacting factor 1 (CRIF1) on the apoptosis of mouse cardiomyocytes (MCMs) induced by palmitic acid. METHODS: The MCMs cultured with medium containing palmitic acid at 0 and 300 μmol/L for 24 h were divided into control group and palmitic acid group, respectively. In order to explore the effects of CRIF1 on MCMs injuries induced by high fat, MCM exposed to palmitic acid at 300 μmol/L for 24 h were divided into vehicle group, scrambled (Scra) siRNA group and CRIF1 siRNA group. The cells in vehicle group were only treated with transfection reagent, the cells in Scra siRNA group were given a treatment with transfection reagent and scrambled RNA, and the cells in CRIF1 siRNA group were given a treatment with transfection reagent and CRIF1 specific siRNA. In order to further confirm the specific mechanism of CRIF1 in high fat-induced MCM injuries, MCMs in CRIF1 siRNA group were divided into DMSO group and N -acetyl cysteine (NAC) group, and were given the same intervention of palmitic acid. RT-qPCR, Western blot and immunofluorescence staining were used to detect the mRNA and protein expression of CRIF1. The apoptotic rate was analyzed by flow cytometry, and the level of intracellular reactive oxygen species (ROS) was tested by DHE staining and ELISA. RESULTS: The expression of CRIF1 was significantly increased after exposure to palmitic acid (P <0.05). Compared with control group, the apoptotic rate was increased significantly in vehicle group and Scra siRNA group (P <0.05). The apoptotic rate was significantly increased in CRIF1 siRNA group (P <0.05). Compared with control group, the intracellular ROS content was significantly increased in vehicle group and Scra siRNA group (P <0.05). Compared with vehicle group and Scra siRNA group, the intracellular ROS content was significantly increased in CRIF1 siRNA group (P <0.05). Compared with DMSO group, the intracellular ROS content and the apoptotic rate were remarkably decreased in NAC group (P <0.05). CONCLUSION: With the inhibition of oxidative stress, CRIF1 may reduce the apoptosis of MCMs induced by high fat. 相似文献
17.
AIM To investigate the expression of histone chaperone anti-silencing function 1B （ASF1B） in prostate cancer cells and its effect on cell viability in vitro . METHODS Human prostate cancer PC-3 cells were used, and knockdown of ASF1B was conducted by small interfering RNA （siRNA） transfection into the cells. The cells were divided into control group, siRNA negative control vector （mock） group and siRNA-ASF1B group. The viability of the PC-3 cells treated with ASF1B-siRNA for 12, 24 and 48 h was measured by MTT assay. Flow cytometry was used to analyze cell apoptosis and cell cycle distribution. The mRNA expression of apoptosis-related molecules was detected by RT-qPCR, and the expression levels of MAPK/JNK/ERK signaling pathway-related proteins were determined by Western blot. RESULTS The protein level of ASF1B in the normal cells （benign prostatic hyperplasia） was significantly lower than that in the PC-3 cells （P <0.01）. Compared with control group and mock group, the protein expression level of ASF1B in the PC-3 cells transfected with siRNA-ASF1B plasmid and the viability of the PC-3 cells were significantly decreased （P <0.01）. The apoptotic rate of the PC-3 cells transfected with siRNA-ASF1B plasmid was significantly higher than that in control group （P <0.01）, and the cell cycle was arrested at G1 phase. The mRNA levels of p53, caspase-3, Bax and PARP-1 in the PC-3 cells transfected with siRNA-ASF1B plasmid were up-regulated compared with those in control group and Mack group （P <0.01）. In addition, the protein levels of MAP2K4 and p-JNK in the PC-3 cells in siRNA-ASF1B group were significantly higher than those in mock group （P <0.01）, while the protein level of p-ERK was significantly lower than that in mock group （P <0.01）. CONCLUSION ASF1B silencing induces G1 arrest and promotes apoptosis of PC-3 cells. Activating MAPK/JNK/ERK signaling pathway may be a possible contributor to the anti-prostate cancer effect of siRNA-ASF1B. 相似文献
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AIM To investigate the effect of sinomenine (SN) on the damage of human neuroblastoma SK-N-SH cells induced by 1-methyl-4-4 phenylpyridine (MPP+) and its mechanism for exploring the pathogenesis of Parkinson disease. METHODS SN was used to treat MPP+-induced SK-N-SH cells. The levels of malondialdehyde (MDA) and glutathione (GSH) in cell culture supernatants were measured by ELISA. The apoptosis was analyzed by flow cytometry. The protein expression levels of Bcl-2 and Bax were determined by Western blot. The expression levels of long noncoding RNA ANRIL and microRNA-626 (miR-626) were detected by RT-qPCR. Dual-luciferase reporter assay was used to evaluate the relationship between ANRIL and miR-626. After ANRIL small interfering RNA was transfected into SK-N-SH cells, the effects of ANRIL expression knock-down on MPP+-induced SK-N-SH cell apoptosis, the protein expression levels of Bcl-2 and Bax, and the levels of MDA and GSH in cell culture supernatants were examined. RESULTS After treatment with MPP+, the apoptotic rate, Bax protein level and ANRIL expression in SK-N-SH cells were increased (P <0.05), and the Bcl-2 protein level and miR-626 expression were decreased (P <0.05). The level of MDA in cell culture supernatants was increased (P <0.05), and the level of GSH was decreased (P <0.05). After SN treatment or ANRIL expression knock-down, decreased apoptotic rate, Bax protein level and ANRIL expression (P <0.05), and increased Bcl-2 protein level and miR-626 expression in MPP+-induced SK-N-SH cells were observed (P <0.05). The level of MDA in the cell culture supernatants was decreased (P <0.05), and the level of GSH was increased (P <0.05). CONCLUSION SN attenuates MPP+-induced damage in SK-N-SH cells by regulating ANRIL/miR-626 signaling pathway. 相似文献