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1.
AIM: To investigate the role of nitric oxide synthase (NOS), soluble guanylyl cyclase (sGC) and protein kinase C (PKC) signaling in tumor necrosis factor-α (TNF-α)-induced cardioprotection against hypoxia/reoxygenation (H/R) injury. METHODS: Neonatal rat ventricular myocytes were pretreated with TNF-α or sodium nitroprusside (SNP) or L-arginine (L-Arg), respectively, for 12 h and then subjected to continuous hypoxia for 12 h, followed by reoxygenation for 6 h. The manganese superoxide dismutase (Mn-SOD) activity of the cells was measured after H/R. Myocyte injury was determined by the release of lactic dehydrogenase (LDH). RESULTS: TNF-α (105 U/L) significantly increased the Mn-SOD activity and decreased release of LDH from ventricular myocytes. The cardioprotection against H/R injury was induced by the pretreatment with SNP (5 μmol/L) or L-Arg (5 mmol/L), which was blocked by ODQ (10 μmol/L), the specific sGC inhibitor, and Chel (5 μmol/L), the specific PKC inhibitor. Pretreatment with L-NAME (100 μmol/L), ODQ, Chel, antoxidant 2-MPG (400 μmol/L) or tyrosine kinase inhibitor genistein (50 μmol/L) attenuated the increased Mn-SOD activity and reduced LDH level induced by TNF-α. CONCLUSION: The results suggest that NO may play a role in TNF-α-induced cardioprotection, which is mediated by sGC and PKC.  相似文献   

2.
AIM:To investigate the effects of phytoestrogen α-zearalanol (ZAL) on hypoxia/reoxygenation (H/R) injury and mechanism involved in human umbilical vein endothelial cells (HUVECs). METHODS:HUVECs were exposed to hypoxia for 3 hours and then reoxygenation 1 hour. ZAL or 17β-estradiol (E2) at concentrations of 10-9-10-6 mol/L were pretreated before hypoxia. The survival rate of HUVECs was detected by MTT. Either the activities of LDH and SOD or the level of MDA in supernatant was detected by spectrophotometry. RESULTS:The survival rate of HUVECs and the activity of SOD were significantly decreased (P<0.01), while the activity of LDH and the level of MDA were significantly increased (P<0.01) after H/R. These changes were reversed by pretreatment with ZAL or E2, and there was no significant difference between their effects in the same dose of ZAL and E2. CONCLUSION:These results suggest that phytoestrogen ZAL protects HUVECs from H/R injury by inhibiting the oxidative stress, which was similar to E2.  相似文献   

3.
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4.
AIM: The aim of this work is to investigate the protective effects of Ginsenoside Rb1 (Rb1) on apoptosis induced by hypoxia/hypoglycemia and reoxygenation in cultured rat hippocampal neurons. METHODS: Apoptosis were measured by flow cytometry; Morphological changes and neuronal necrosis were examined under microscope; The leakage of lactic dehydrogenase (LDH) and the product of nitric oxide (NO) were measured. RESULTS: hypoxia/hypoglycemia cultures for 5 h and reoxygenation induced neuronal apoptosis and necrosis,and significantly increased the leakage of LDH and the product of NO. The effects were enhanced with the extending time of reoxygenation. Rb1 could significantly decrease the percentage of neuronal apoptosis and necrosis, and reduce the leakage of LDH and the product of NO. CONCLUSION: Rb1 had an effect of anti-neuronal apoptosis. This effect might be related to the inhibition of the activity of NO synthase and NO production.  相似文献   

5.
AIM： To investigate the effects of Panax quinquefolium saponins (PQS) and calcineurin (CaN) signal pathway on cardiomyocyte injury induced by myocardial hypoxia/reoxygenation(H/R). METHODS：Cultured cardiomyocytes isolated from neonatal Sprague-Dawley rats were used to establish the H/R model. The cells were transfected with pCDB-CaN plasmid to overexpress CaN, or exposed to the CaN inhibitor FK506 to interfere the CaN expression. The cardiomyocytes were divided into control group, H/R group, PQS+H/R group, CaN+PQS+H/R group, pCDB+PQS+H/R group and FK506+PQS+H/R group. The apoptosis was analyzed by flow cytometry. The activity of CaN in the cardiomyocytes was detected. The protein expression of CaN was determined by Western blotting. RESULTS：Compared with control group, the apoptosis of the cardiomyocytes in CaN group was significantly increased. Compared with PQS+H/R group, the cell apoptosis, the expression of Bcl-2 and Bax, the activity of CaN and its protein expression in FK506 group were not significantly different. CONCLUSION：Inhibition of CaN activity reduces the H/R injury in cardiomyocytes. However, the mechanism of PQS protecting cardiomyocytes from H/R injury may not be associated with the CaN signaling pathway.  相似文献   

6.
AIM: To investigate the effect of Ca2+/calmodulin-dependent protein kinase Ⅱ (CaMKⅡ) on hypoxia/reoxygenation (H/R) injury in H9c2 cells. METHODS: H9c2 cells were randomized into 4 groups:control group, KN-93 (an inhibitor of CaMKⅡ; 1 μmol/L) treatment group, H/R group and H/R+KN-93 (1 μmol/L) treatment group. The cells in KN-93 group and KN-93+H/R group were pretreated with KN-93 for 2 h before the other treatment was performed. The viability of H9c2 cells in each group was measured by CCK-8 assay. Lactate dehydrogenase (LDH) activity in the culture medium was detected. The protein levels of phosphorylated CaMKⅡ (p-CaMKⅡ), phosphorylated phospholamban (p-PLN) and cleaved caspase-3 were determined by Western blot. The apoptosis was analyzed by TUNEL staining and the flow cytometry. RESULTS: No significant difference of all indexes tested between control group and KN-93 group was observed. H/R treatment significantly reduced the cell viability, and increased the activity of LDH (P<0.01), the protein levels of p-CaMKⅡ, p-PLN and cleaved caspase-3 (P<0.05), and the apoptotic rate (P<0.01). KN-93 (1 μmol/L) significantly increased the cell viability, and decreased the activity of LDH (P<0.01), the protein levels of p-CaMKⅡ, p-PLN and cleaved caspase-3 (P<0.05), and the apoptotic rate (P<0.01). CONCLUSION: CaMKⅡ aggravates hypoxia/reoxygenation injury in the H9c2 cells by activating apoptosis.  相似文献   

7.
AIM: To investigate the effect of hesperetin on hypoxia/reoxygenation (H/R)-induced apoptosis in the H9c2 cells and to clarify the underlying mechanism. METHODS: The H/R model was established and the H9c2 cells were pretreated with hesperetin for 4 h. The cell viability and cell damage were measured by CCK-8 assay and lactate dehydrogenase (LDH) detection. The apoptosis was analyzed by Hoechst 33258 staining and flow cytometry. The intracellular calcium fluorescence intensity was measured by fluorescence microscopy and flow cytometry. The calcium-ATPase activity and the level of adenosine triphosphate (ATP) were measured by ELISA. The mitochondrial membrane potential was measured by JC-1 staining. The protein expression levels of Bcl-2, Bax and cytochrome C (Cyt-C) were determined by Western blot. RESULTS: Hesperetin reduced the apoptosis of the H9c2 cells induced by H/R, decreased intracellular Ca2+ fluorescence intensity, elevated Ca2+-ATPase activity, inhibited the mitochondrial membrane potential depolarization and increased the level of ATP (P<0.05). In addition, hesperetin significantly reduced the release of Cyt-C protein from mitochondria to cytoplasma and increased the Bcl-2/Bax ratio (P<0.05). After using the calcium ion inhibitor nimodipine, the percentage of the cells with mitochondrial membrane depolarization was decreased, the ATP level was increased and the protein expression of mitochondrion-related apoptosis molecules were decreased (P<0.05). CONCLUSION: Hesperetin reduces the apoptosis of the H9c2 cells induced by H/R, which may be related to inhibition of calcium overload and improvement of mitochondrial function.  相似文献   

8.
《园艺学报》是中国园艺学会和中国农业科学院蔬菜花卉研究所主办的学术期刊,创刊于1962年,刊载有关果树、蔬菜、观赏植物、茶及药用植物等方面的学术论文、研究报告、专题文献综述、问题与讨论、新技术新品种以及园艺研究动态与信息等,适合园艺科研人员、大专院校师生及农业技术推广部门专业技术人员阅读参考。《园艺学报》是中文核心期刊,被英国《CAB文摘数据库》、美国CA化学文摘、日本CBST科学技术文献速  相似文献   

9.
AIM: To investigate the effect of polysaccharide from Fructus corni(PFC) on cardiomyocytes against hypoxia/reoxygenation (H/R) injury and its possible relationship with ROS/PKC/p38 MAPK pathway.METHODS: Primary cardiomyocytes were isolated from neonatal SD rats and randomly divided into normal group, H/R group, PFC (20 mg/L, 100 mg/L and 200 mg/L) preconditioning+H/R groups, chelerythrine+PFC (100 mg/L)+H/R group and SB203580+PFC (100 mg/L)+H/R group. The cell viability was measured by inverted microscopic observation. Apoptosis in the cardiomyocytes was detected by Hoechst 33258 staining and fluorescence microscopy. The levels of lactate dehydrogenase (LDH) and superoxide dismutase (SOD) in the cell culture supernatants, and the reactive oxygen species (ROS) in the cells were also measured by microplate reader. The protein levels of PKC, p-p38 MAPK and HSP70 in the cells were detected by Western blotting.RESULTS: Compared with normal group, the cell viability and beating frequency were decreased in H/R group. LDH and ROS contents, apoptotic rate and p-p38 MAPK level increased significantly (P<0.01). Compared with H/R group, PFC preconditioning increased beating frequency, SOD activity and the protein level of PKC and HSP70, and decreased ROS production, the protein level of p-p38 MAPK and cell apoptotic rate. However, the effect of PFC was inhibited by chelerythrine or SB203580.CONCLUSION: PFC may protect cardiomyocytes from hypoxia/reoxygenation injury. Its mechanism is possibly involved in the inhibition of ROS via increasing the activity of SOD and the activation of PKC, and suppression of excessive activation of p38 MAPK.  相似文献   

10.
AIM:To investigate the effects of hypoxia/reoxygenation (H/R) for different reoxygenation times on cardiomyocyte injury. METHODS:Human cardiomyocyte AC16 was cultured in glucose-free and serum-free DMEM with 1% O2 for 24 h, 10% fetal bovine serum and low glucose DMEM combined with 21% O2 were used to establish reoxygenation for 2 h, 6 h and 12 h, respectively. The cell viability was measured by CCK-8 assay. The protein levels of different cell injury pathway related molecules, such as LC3-Ⅱ/-I (autophagy), caspase-1 and gasdermin D (pyroptosis) and caspase-3 and Bax/Bcl2 (apoptosis), were determined by Western blot. RESULTS:Compared with blank control group, the cell viability in each H/R group was continuously decreased with the extension of reoxygenation time (P<0.05). The expression of LC3-Ⅱ/-I was up-regulated in hypoxia group and H/R group compared with blank control group (P<0.05). In addition, the protein levels of cleaved caspase-1 and cleaved gasdermin D were increased in H/R groups for 6 h and 12 h, respectively (P<0.05). Cleaved caspase-3 and Bax/Bcl2 were increased after reoxygenation for 12 h (P<0.05). CONCLUSION:Autophagy in hypoxia-induced AC16 cells is up-regulated, and then decreased by reoxygenation. The cell pyroptosis is activated earlier than the apoptosis during reoxygenation.  相似文献   

11.
AIM: To investigate the protective effect of calcium antagonists on anoxia/reoxygenation (A/R) injury of cardiomyocytes. METHODS: Primary-cultured cardiomyocytes were divided into four groups, namely A/R, A/R+nifedipine (Nif), A/R+ruthenium red (Ru)+heparin (Hep) and control groups. The following parameters were measured in all groups: intracellular calcium concentration (i), cardiac cell viability, ATP content, lactate dehydrogenase (LDH) activity in the medium, PKC and MAPK activity and 3[H]-Leucine (3[H]-Leu) incorporation. RESULTS: In comparison with A/R group,A/R+nifedipine (Nif) and A/R+ruthenium red (Ru)+heparin (Hep) groups showed a marked decrease in[Ca2+]i and LDH content,and a significant increase in cell viability, ATP content, activity of PKC and MAPK and [3H]-Leu incorporation (P<0.05 or P<0.01). CONCLUSION: A/R mediated Ca2+ overload resulted in cardiomyocyte injury, which could be attenuated by blocking Ca2+ entry and release.  相似文献   

12.
AIM：To elucidate whether ZFP580 is involved in the cardioprotective effects of hypoxic preconditioning (HPC) against hypoxia-reoxygenation (H/R) injury in H9c2 myocardial cells. METHODS：Rat heart-derived H9c2 cells were cultured in DMEM. H/R was induced by incubation under ischemic hypoxia for 3 h and reoxygenation for 2 h. HPC was induced by exposing the H9c2 cells to 10 min of hypoxia and 20 min of reoxygenation for 3 cycles before H/R treatment. MTT staining and LDH leakage detection were used to evaluate the effects of HPC. Western blotting was used to detect the protein levels of ZFP580, phosphorylated ERK1/2 and cleaved caspased-3. The effects of ZFP580 overexpre-ssion or knockdown on H/R induced apoptosis were determined. RESULTS：The results of MTT staining and LDH leakage detection showed evidence of HPC cytoprotection against H/R-induced cell death in H9c2 cells. ZFP580 protein level and ERK1/2 phosphorylation were significantly increased in the HPC group compared with control group and H/R group. PD98059, an inhibitor of ERK1/2 phosphorylation, significantly suppressed the HPC-induced up-regulation of ZFP580 protein expression. ZFP580 overexpression significantly inhibited apoptosis and caspase-3 activation in H9c2 cells. CONCLUSION：HPC exhibits cytoprotection against H/R and leads to high level of ZFP580 protein in H9c2 cells. ZFP580 is regulated by ERK1/2 activation and mediates the anti-apoptotic effect of the ERK1/2 signaling pathway in HPC cytoprotection.  相似文献   

13.
AIM: To observe the effects of acetal hairy holly extractive compound R4(AHHECR4) on myocardial cell injury induced by hypoxia/reoxygenation. METHODS: The model of rat myocardial cell injury was induced by hypoxia/reoxygenation. The activity of superoxide dismutase (SOD) in the myocardial cells was measured by the method of xanthine oxidase. The content of malondialdehyde (MDA) was determined by the method of thiobarbituric acid. The activity of dehydrogenase (A) in mitochondria was detected by MTT assay. The activity of lactate dehydrogenase(LDH) and the content of NO in the culture medium were also evaluated. RESULTS: AHHECR4 at concentrations of 5, 10 and 20 μmol/L remarkably increased SOD activity and the value of A, and significantly inhibited MDA production and LDH leakage. Greatly increased content of NO in the culture medium was also observed. CONCLUSION: The results indicate that AHHECR4 has a protective effect on myocardial cells under the condition of hypoxia/reoxygenation injury.  相似文献   

14.
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   

15.
AIM: To investigate whether tumor necrosis factor α (TNFα) pretreatment can inhibit mitochondrial permeability transition pore opening in isolated rat hearts subjected to hypoxia and reoxygenation. METHODS: Isolated perfused rat hearts were subjected to 30 min regional hypoxia (occlusion of left anterior descending artery) and 120 min reoxygenation. The infarct size, lactate dehydrogenase (LDH) release during reoxygenation and ventricular hemodynamic parameters were measured. RESULTS: Pretreatment with TNFα at concentration of 1×104 U/L for 7 min followed by 10 min washout reduced the infarct size and LDH release, and improved the left ventricular performance (left ventricular developed pressure and rate-pressure product) and left ventricular end-diastolic pressure during hypoxia and reoxygenation. Administration of atractyloside (Atr, an opener of mitochondrial permeability transition pore, 20 μmol/L) for 20 min (last 5 min of hypoxia and first 15 min of reoxygenation) and paxilline (Pax, a calcium activated potassium channel antagonist, 1 μmol/L) for 5 min before hypoxia attenuated the reduction of infarct size and LDH release and improved the left ventricular performance induced by TNFα. CONCLUSION: The findings indicate that in the isolated rat heart model, TNFα protects myocardium against hypoxia and reoxygenation injury via inhibiting mitochondrial permeability transition pore opening as well as activating calcium, activated potassium channel.  相似文献   

16.
AIM: To study the effects of anti-aging Klotho protein on neonatal rat myocardial cells with hypo-xia/reoxygenation (H/R) injury. METHODS: The cardiomyocytes of neonatal SD rats were cultured to establish hypoxia/reoxygenation model. The myocardial cells were divided into normal control group, H/R model group, different concentrations of Klotho protein (0.1 μmol/L, 1 μmol/L and 10 μmol/L) pretreatment groups. The myocardial cells pulse frequency was observed before and after H/R. The cell viability was measured by MTT assay. The leakages of LDH, CK and AST, the content of MDA and the activity of SOD were detected. The apoptotic rate of the myocardial cells was analyzed by flow cytometry. The mRNA expression of endoplasmic reticulum stress markers and apoptosis-related molecules GRP78, CRT, CHOP and caspase-12 was measured by real-time PCR. The protein levels of CHOP, caspase-12 and phosphorylated Akt in the myocardial cells were determined by Western blot. RESULTS: Compared with normal control group, the pulse frequency, cell viability rate and SOD activity of myocardial cells were significantly decreased, the cell apoptotic rate as well as the contents of LDH, CK, AST and MDA were increased in H/R model group. The mRNA expressions of GRP78, CRT, CHOP and caspase-12 as well as the protein levels of CHOP and caspase-12 were increased, whereas p-Akt level was decreased obviously. Compared with H/R model group, the pulse frequency, cell viability rate and SOD activity were increased significantly, the cell apoptotic rate as well as the contents of LDH, CK, AST and MDA were decreased in Klotho pretreated group. The mRNA expression of GRP78, CRT, CHOP and caspase-12 as well as the protein levels of CHOP and caspase-12 were decreased, while p-Akt level increased significantly. CONCLUSION: Anti-aging Klotho protein improves the myocardial cell survival and inhibits the apoptosis by increasing the resistance of the cells to oxidative stress and excessive endoplasmic reticulum stress response, which is related with the activation of Akt phosphorylation in H/R-injured mycardial cells.  相似文献   

17.
AIM: To investigate the neuroprotective effect of Ganoderma lucidum extract (GLE) in an in vitro model of primary cultured neurons with oxygen and glucose deprivation (OGD). METHODS: Neuronal injury was induced by oxygen and glucose deprivation/reoxygenation (OGD/R). The neuronal injury and viability were determined by LDH leakage and XTT assay at 0 h,3 h,6 h,12 h,24 h,48 h and 72 h after OGD/R. Neuronal apoptosis was detected by flow cytometry (FCM). The expression of apoptosis-related proteins was analyzed by Western blotting.RESULTS: The viability of the neurons increased with exposure to GLE (0.1 mg/L,1 mg/L and 10 mg/L)after OGD/R. The LDH releases were also significantly reduced. GLE significantly inhibited OGD/R-induced apoptosis of cultured rat cortical neurons in a concentration-dependent and time-dependent manner(P<0.05). GLE at concentrations of 0.1 mg/L,1 mg/L and 10 mg/L inhibited the expression of caspase-3 and caspase-8 proenzyme. Additionally,GLE at concentration of 10 mg/L suppressed the expression of caspase-9 proenzyme.CONCLUSION: Our findings provide the evidence that the GLE has neuroprotective effect on cerebral ischemia. The mechanisms are related to the inhibition of caspase-3,-8 and-9 activations. GLE may be a novel and effective reagent for treating ischemic stroke.  相似文献   

18.
AIM: To investigate the changes of endogenous cystathionine-γ-lyase/hydrogen sulfide pathway on hypoxia/reoxygenation injury in vivo and to explore the relationship between this pathway and hypoxia/reoxygenation injury. METHODS: Primary myocardial cell culture in vivo came from Wistar baby rats born less than 48 h. The cells were under the conditions of hypoxia (2% O2, 5% CO2) for 3 h and reoxygenation (21% O2, 5% CO2) for 2 h to induce hypoxia/reoxygenation injury. MTT was used to detect the cell survival in every group. The activities of lactate dehydrogenase (LDH) in culture medium, malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial cells were measured with colorimetry method. RT-PCR method was used to test CSE mRNA expression in myocardial cells. RESULTS: Compared to IR group, the cells in NaHS+IR and IR+NaHS groups had a higher survival rate, lower LDH concentration in culture medium, higher SOD activity and lower MDA in myocardial cells. At the same time, the results of RT-PCR displayed that CSE mRNA were down-regulated in myocardial cells after hypoxia/reoxygenation injury, and if CSE inhibitor PPG was added into the culture medium before hypoxia, no protective effects were detected. CONCLUSION: NaHS might protect the myocardial cells from hypoxia/reoxygenation injury through decreasing oxygen free radical production and stabilizing the cell membrane.  相似文献   

19.
AIM: To demonstrate the mechanisms underlying cardioprotection induced by ischemic postconditioning (I-postC) via studying the alteration of calreticulin (CRT)/calcineurin (CaN) signaling pathway in rat heart subjected to ischemia/reperfusion (I/R).METHODS: The model of myocardial I/R injury in vivo was made by occluding the left anterior descending artery for 45 min followed by 24 h of reperfusion in Wistar rats.Hemodynamics and activity of lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB) in plasma were measured.Myocardial infarct size was measured by 2,3,5- triphenyltetrazolium chloride (TTC) staining and cardiomyocyte apoptosis was detected using in situ TDT-mediated dUTP nick end labeling (TUNEL).The activity of CaN,the expressions of CaN and CRT in myocardium were detected by enzyme reaction phosphorus measurement and Western blotting analysis,respectively.RESULTS: Cyclosporin A,the inhibitor of CaN,limited significantly myocardial infarct size and cardiomyocyte apoptosis induced by I/R,but had no significant effect on cardiac function.I-postC ameliorated significantly the cardiac dysfunction induced by I/R.Compared with those in I/R group,the myocardial infarct size,the LDH and CK-MB activities in plasma and the cardiomyocyte apoptotic index were significantly reduced in I-postC group.In addition,I/R-induced upregulation of CaN activity,CaN and CRT expression were relieved by I-postC.No significant difference was found between I-postC and ischemic preconditioning groups.I-postC had stronger protective effect on the reperfused heart compared with cyclosporin A.CONCLUSION: The findings indicate that I-postC protects myocardium against I/R injury,at least in part,via inhibiting the CRT/CaN signaling pathway.  相似文献   

20.
AIM: To study the effect of Tribulus terrestris L. saponin (TTLS) on apoptosis and changes in cytosolic calcium concentration induced by hypoxia/re-oxygenation in rat cortical neurons. METHODS: Rat cortical neurons in primary culture were used, and a apoptosis model was induced by hypoxia/reoxygenation. LDH releasing rate was detected by spectrophotometry. The apoptosis rate of cortical neurons was analyzed quantitatively by flow cytometry with Annexin V-FITC and PI staining. Intracellular free Ca2+(［Ca2+］i) was observed with a confocal laser-scanning microscope and determined by mean fluorescent value with Fluo-3 fluometry. RESULTS: Compared to control group, three hours of hypoxia and twelve hours of reoxygenation group induced cortical neuronal apoptosis and significantly increased the intracellular free Ca2+ concentration（P<0.01). Compared with model group, TTLS decreased the percentage of neuronal apoptosis and reduced neuronal ［Ca2+］i（P<0.01).CONCLUSION: TTLS could obviously reduce hypoxia/reoxygenation-induced apoptosis and alleviate the damage degree of rat cortical neurons.The mechanism might be related to inhibiting the calcium overload induced by hypoxia/reoxygenation in rat cortical neurons.  相似文献   

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