共查询到20条相似文献，搜索用时 55 毫秒
1.
AIM: To investigate the effect of acetyl-L-carnitine (ALC) on H2O2-induced oxidative damage in PC12 cells and its possible mechanism. METHODS: A moderate oxidative damage PC12 cell model was induced by exposure of the PC12 cells to H2O2. ALC at different concentrations (100, 200 and 400 μmol/L) was applied to the PC12 cells cultured in vitro, and CCK8 assay was used to detect the cell viability. The cells were divided into control group, H2O2 group, and low-ALC, medium-ALC and high-ALC groups. The apoptosis of the cells was analyzed by flow cytometry. The protein levels of Nrf2 and cleaved caspase-3 were determined by Western blot. The nuclear translocation of Nrf2 was observed by immunofluorescence staining. RESULTS: ALC at different concentrations (100, 200 and 400 μmol/L) significantly inhibited H2O2-induced PC12 cell apoptosis, and the medium concentration group had the best effect. Compared with H2O2 group, low, medium and high concentrations of ALC significantly increased the viability of the PC12 cells induced by H2O2, inhibit cell apoptosis (P<0.05), significantly down-regulated the protein level of cleaved caspase-3 (P<0.05), up-regulated the protein level of Nrf2 (P<0.05), and promoted the translocation of Nrf2 from the cytoplasm to the nucleus. CONCLUSION: Acetyl-L-carnitine attenuates H2O2-induced oxidative damage of PC12 cells, inhibits the apoptosis and increases the viability, which is related to the activation of Nrf2 signaling pathway. 相似文献
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AIM:To investigate the effect of shikonin on the apoptosis and oxidative stress induced by high concentration of glucose in vascular endothelial cells. METHODS:Rat thoracic aortic endothelial cells were randomly divided into 5 groups:normal control group (with glucose at concentration of 5.5 mmol/L in cell culture medium), high glucose group (with glucose at concentration of 33 mmol/L in cell culture medium), high glucose+low shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 0.1 μmol/L in cell culture medium), high glucose+medium shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 1 μmol/L in cell culture medium), and high glucose+high shikonin group (with glucose at concentration of 33 mmol/L and shikonin at concentration of 10 μmol/L in cell culture medium). After treatments, the cell viability was measured by CCK-8 assay and cell apoptotic rate was analyzed by flow cytometry. In addition, the status of oxidative stress was evaluated by determining the levels of malondialdehyde (MDA), reactive oxygen species (ROS), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). The activation of Nrf2/HO-1 signaling pathway was determined by Western blot. RESULTS:Compared with high glucose group, shikonin reversed high glucose-induced decrease in cell viability and increase in apoptosis in a concentration-dependent manner. High concentration of glucose induced high levels of MDA and ROS, while decreased the levels of SOD and GSH-Px. However, after treatment with shikonin, the contents of MDA and ROS were decreased, while the activities of SOD and GSH-Px were increased as compared with high glucose group. Furthermore, the high concentration of glucose up-regulated the protein levels of cleaved caspase-3, HO-1 and Nrf2 (nuclear). Compared with high glucose group, the protein levels of cleaved caspase-3, HO-1 and Nrf2 (nuclear) were partly decreased after treatment with shikonin. CONCLUSION:Shikonin alleviates high glucose-induced vascular endothelial cell apoptosis. Its mechanism may be related to activation of Nrf2/HO-1 signaling pathway and down-regulation of oxidative stress in vascular endothelial cells. 相似文献
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AIM To study the effect of microRNA-153-3p (miR -153 -3p ) knock-down on oxidative injury of H9C2 cells induced by H2O2 and its specific mechanism. METHODS The oxidative stress injury of H9C2 cell model was induced by H2O2, and then the cell viability and the expression of miR-153-3p were detected by MTT assay and RT-qPCR, respectively. The effects of miR -153 -3p knock-down on the H9C2 cell injury under oxidative stress were studied by RNA interference technology. The targets of miR-153-3p were identified by Western blot and dual-luciferase reporter assay. RESULTS MTT assay showed that the viability of H9C2 cells was decreased with the increase in H2O2 concentration (P< 0.05). The results of RT-qPCR showed that the expression of miR-153-3p was increased with the increase in H2O2 concentration (P< 0.05). Knock-down of miR -153 -3p increased the viability of H9C2 cells under oxidative stress, decreased the cell apoptosis and the content of malondialdehyde (MDA), and increased the activity of superoxide dismutase (SOD). The expression of nuclear factor E2-related factor 2（Nrf2） and antioxidant response element（ARE） activity were increased with the increase in H2O2 concentration (P< 0.01). TargetScan analysis and dual-luciferase reporter assay showed that Nrf2 was one of the potential target genes of miR-153-3p. The results of Western blot further showed that over-expression of miR-153-3p inhibited the expression of Nrf2 (P< 0.01), while down-regulation of miR-153-3p increased the expression of Nrf2 (P< 0.01). Dual interference with Nrf2 and miR -153 -3p significantly reduced H9C2 cell viability, promoted the apoptosis, increased MDA content, and decreased SOD activity in the presence of H2O2 (P< 0.01). CONCLUSION Inhibition of miR-153-3p expression attenuates the injury of H9C2 cells induced by H2O2 through up-regulating Nrf2/ARE signaling pathway. 相似文献
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AIM: To investigate the effects of naringenin (NAR) on the myocardium as well as its effects on adenosine monophosphate-activated protein kinase (AMPK)/nuclear factor (NF)-E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) signaling pathways in diabetic mice. METHODS: C57BL/6 mice (n=50) were randomly divided into normal group (N group) and model group. The mouse model of type 1 diabetes mellitus was established by intraperitoneal injection of streptozotocin (STZ), then the mice were divided into diabetes group (D group), diabetes+low dose of NAR intervention group (D+L-NAR group), diabetes+middle dose of NAR intervention group (D+M-NAR group) and diabetes+high dose of NAR intervention group (D+H-NAR group). The mice in intervention groups were received NAR at low, middle and high doses respectively by gavage, and the mice in N group and D group were received equal volume of normal saline. After 6 weeks, the mice were sacrificed to observe the effects of NAR at different doses on the body weight and blood glucose. The histopathological changes of the cardiac tissues were observed with HE staining. The myocardial collagen volume fraction (CVF) was calculated by Masson staining. Immumohistochemical staining was used to test the protein levels of interleukin-6 (IL-6) and IL-10, and the TUNEL was used to observe the apoptosis of myocardial tissues. The production of reactive oxygen species (ROS) in the myocardial cells was analyzed by fluorescence probe of DHE, and superoxide dismutase (SOD) activity and malondiodehyde (MDA) content in the myocardial cells were measured by SOD and MDA kits. Western blot was applied to determine the protein levels of p-AMPKα, AMPKα, Nrf2, HO-1, NAD(P)H:quinone oxidoreductase 1 (NQO1) and cleaved caspase-3 in the myocardial tissues. RESULTS: Compared with N group, the blood glucose of the mice in D groups was increased and the body weight was decreased significantly. Compared with D group, the blood glucose of the mice in NAR intervention groups was decreased and the body weight was increased. Compared with N group, the CVF, apoptotic rate and the protein levels of IL-6, cleaved caspase-3 were increased, while the protein levels of IL-10, p-AMPKα, Nrf2, HO-1, NQO1 and SOD activity were decreased, the ROS production rate and MDA content was increased significantly in D group (P < 0.05). Compared with D group, the CVF, apoptotic rate and the protein levels of IL-6, cleaved caspase-3 were relatively decreased, conversely the protein levels of IL-10, p-AMPKα, Nrf2, HO-1, NQO1 were increased in NAR intervention groups(P < 0.05). No significantly difference of the ROS production rate, SOD activity and MDA content between D group and D+L-NAR group was observed. However, the ROS production rate and MDA content was decreased,SOD activity were increased in D+M-NAR group and D+H-NAR group as compared with D group. CONCLUSIONS: NAR attenuates myocardial injury in diabetic mice, and its mechanism may be related to regulation of AMPK/Nrf2/HO-1 signaling pathway, enhancement of the antioxidant reaction, reduction of myocardial fibrosis, apoptosis and inflammation. 相似文献
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AIM:To investigate the effect of cyclophosphamide(CTX) on proliferation and apoptosis of mesangial cells(GMC) of rat in vitro. METHODS:GMC proliferat ion was detected by MTT method,GMC apoptosis was examined by inverted microscopy for phase-contract and fluoroscopy and flow cytometry analysis.The levels of Fas and Bcl-2 were also detected by immunohistology. RESULTS:The proliferation of GMC were inhibited by CTX, methylprednisolone(MP), low molecular weight heparin(LMWH). Apoptosis of GMC was induced by CTX, the apoptosis rate of GMC was 8.2%, and the Fas level was increased. CONCLUSION:CTX could inhibit proliferation and induce apoptosis of GMC possibly by enhancing the Fas level. 相似文献
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ABUDUMIJITI Gu-li-ni-ge-er SHABITI Sha-yi-bai CONG Yuan-yuan ABULIZI Pa-li-da 《园艺学报》2021,37(1):112-118
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AIM: To investigate the effects of ginsenoside RH2 (GS-RH2) on neovascularization of rats with middle cerebral artery occlusion (MCAO) and its potential mechanisms. METHODS: SPF Sprague-Dawley rats were randomly divided into sham operation (sham) group, MCAO model (MCAO) group and GS-RH2 group, with 18 rats in each group. After surgery, the general condition and neurological function score of the rats were assessed. At the 1st day, 3rd day and 7th day after intervention, the microvessel density (MVD), the content of malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were examined. The protein expression of kelch-like ECH-associated protein 1 (Keap1), nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was determined by Western blot. RESULTS: Compared with sham group, the rats in MCAO group showed significant neurobehavioral obstacles and ischemic brain infarction with higher neurological function score, while treatment with GS-RH2 significantly improved behavioral impairment and reduced the infarction volume with lower neurological function score. The MVD score in GS-RH2 group was increased as the animal survival time prolonged, while the MVD score in MCAO group was decreased. After intervention for 7 d, the MVD score in GS-RH2 group was significantly higher than that in MCAO group (P<0.05). Compared with sham group, the content of MDA was increased and the activities of SOD and GSH-Px were decreased in MCAO group at each time point. After intervention for 7 d, the MDA content was decreased and the SOD and GSH-Px activities were increased in GS-RH2 group compared with MCAO group. After intervention for 7 d, the protein expression of Nrf2 and HO-1 was increased, while the protein expression of Keap1 was decreased in GS-RH2 group compared with MCAO group(P<0.05). CONCLUSION: Ginsenoside RH2 promotes neovascularization of MCAO model rats. The mechanism may be related to the activation of Keap1/Nrf2 signaling pathway, promotion of the antioxidant enzyme activity and inhibition of oxidative stress. 相似文献
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AIM: To explore the effect of Yiqi-Yangyin recipe on myocardial ischemia-reperfusion injury (MIRI) in rats with diabetes mellitus (DM) and the possible mechanism. METHODS: The rats were divided into normal group (control group), DM sham operation (DM-S) group, DM+MIRI group, low-, medium-and high-dose Yiqi-Yang-yin recipe (TL, TM and TH) groups (7.5, 15 and 30 g/kg decoction of Yiqi-Yangyin recipe by gavage), and Nrf2 inhibitor (bardoxolone methyl) group (30 mg/kg bardoxolone methyl by intragastric administration). The gavage volume was 1 mL/kg. There were 15 rats in each group, and they were administered continuously for 7 d. The tail vein blood was collec-ted after the last administration to detect the blood sugar and lipid levels in the rats. The serum levels of cardiac troponin I (cTnI), tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-10 were measured by ELISA. Echocardiography was used to detect the changes of cardiac function in the rats after blood collection. After cardiac function test, the rats were sacrificed to obtain cardiac tissues, and the volume changes of myocardial infarction were assessed by triphenylte-trazole chloride staining. The histopathological changes of myocardium was observed by HE staining. The cardiomyocyte apoptosis was determined by TUNEL assay. The protein levels of phosphorylated extracellular signal-regulated kinase (p-ERK), nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) in the myocardium were determined by Western blot. The myocardial activity of superoxide dismutase (SOD) was measured by nitro blue tetrazolium method, the content of malondialdehyde (MDA) was tested by thiobarbituric acid method, and the production of reactive oxygen species (ROS) was analyzed by iron ion reduction method. RESULTS: Compared with control group, the levels of fasting blood glucose (FBG), total cholesterol (TC) and triglyceride (TG) in DM-S group and DM+MIRI group were significantly elevated, while the level of high-density lipoprotein cholesterol (HDL-C) was significantly lowered (P<0.05). Compared with DM-S group and DM+MIRI group, the levels of FBG, TC, TG in TL, TM, TH and bardoxolone methyl groups were significantly decreased, while HDL-C level was significantly increased (P<0.05). Compared with control group and DM-S group, heart rate (HR) and left ventricular end-diastolic pressure (LVEDP) were increased in DM+MIRI group, mean arterial pressure (MAP), left ventricular systolic pressure (LVSP) and left ventricular ejection fraction (LVEF) were decreased, serum levels of cTnI, TNF-α, IL-1β and IL-10 were increased, the myocardial infarction volume percentage was increased, the myocardial cell breakage and necrosis were increased, the myocardial cell apoptotic rate was increased, the protein levels of p-ERK1/2, Nrf2 and HO-1 were decreased, MDA and ROS levels were increased, and the activity of SOD was decreased (P<0.05). Compared with DM+MIRI group, HR and LVEDP were decreased in TL, TM, TH and bardoxolone methyl groups, MAP, LVSP and LVEF were increased, the serum levels of cTnI, TNF-α, IL-1β and IL-10 were decreased, the myocardial infarction volume percentage was decreased, myocardial cell breakage and necrosis were decreased, myocardial cell apoptotic rate was decreased, the protein levels of p-ERK1/2, Nrf2 and HO-1 were increased, the MDA and ROS levels were decreased, and the activity of SOD was increased (P<0.05). CONCLUSION: Yiqi-Yangyin recipe protects the myocardial tissue of DM+MIRI rats from injury and reduces the oxidative stress level, which may be achieved by activating ERK/Nrf2/HO-1 pathway. 相似文献
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AIM: To investigate the role of zerumbone (ZER) in 1-methyl-4-phenylpyridinium (MPP+)-induced cytotoxicity of human neuroblastoma SH-SY5Y cells. METHODS: Human neuroblastoma SH-SY5Y cells were cultured in vitro and the protective effect of ZER against MPP+-induced cytotoxicity was measured by CCK-8 assay. Flow cytometry was used to determine the apoptosis and reactive oxygen species (ROS). The expression of Parkinson disease protein 7 (PARK7) was knocked-down by using PARK7-specific short hairpin RNA (shRNA). The protein levels of PARK7, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were determined by Western blot. RESULTS: MMP+ remarkably reduced the cell viability in a dose-dependent and time-dependent manner. The SH-SY5Y cell injury model was established by treatment with MPP+ at 600 μmol/L for 24 h. ZER up-regulated the protein levels of PARK7 and Nrf2 (P<0.05), alleviated apoptosis (P<0.05), and reduced ROS production (P<0.05) in the SH-SY5Y cell injury model. Meanwhile, N-acetyl-L-cysteine (NAC) had the similar functions. Moreover, significant reductions in the protein levels of Nrf2 and HO-1 (P<0.05), and obvious increases in apoptosis (P<0.05) and ROS level (P<0.05) were demonstrated in PARK7-knockdown cells. CONCLUSION: ZER protects SH-SY5Y cells against MPP+-induced cytotoxi-city, which may be related to activation of PARK7/Nrf2/HO-1 pathway, and subsequent attenuation of oxidative stress and apoptosis. 相似文献
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AIM: To investigate the effect of salvianolate on oxidative damage induced by hydrogen peroxide in human endothelial EA.hy926 cells.METHODS: EA.hy926 cells were cultured in vitro and divided into the following groups:control group, damage group, and anti-damage groups (salvianolate+damage groups). The cell viability was measured by CCK-8 assay. The migration ability of the EA.hy926 cells was detected by Transwell assay. The content of nitric oxide (NO) in the culture supernatant of the EA.hy926 cells was examined. The levels of vascular endothelial growth factor (VEGF) were detected by ELISA. The apoptosis,mitochondrial membrane potential and intracellular superoxide anion content of the EA.hy926 cells were analyzed by flow cytometry. The protein levels of caspase-3, cleaved caspase-3, Bcl-2, Bax, NF-κB and p53 were determined by Western blot. RESULTS: Compared with damage group, the viability of EA.hy926 cells pretreated with salvianolate at different concentrations was significantly increased (P<0.05). The apoptotic rate was significantly decreased (P<0.05). Savianolate enhanced the migration ability of the cells. The levels of VEGF, NO and mitochondrial transmembrane potential were increased (P<0.05), and the intracellular ROS level was significantly decreased (P<0.05). The protein levels of NF-κB, p53, Bax and cleaved caspase-3 were significantly decreased, and the protein level of Bcl-2 was markedly increased(P<0.05). CONCLUSION: Savianolate reduces the damage of EA.hy926 cells by hydrogen peroxide exposure, and its mechanism may be related to the blocking of NF-κB signaling pathway. 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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ZHANG Yi-min YE Ren-gao LI You-ji LI Xiao-yan WANG Chang-yun YU Xue-qing DONG Xiu-qing 《园艺学报》2007,23(9):1796-1800
AIM: To study the effects and mechanism of recombinant human defensin α1 on cell proliferation in cultured rat glomerular mesangial cells.METHODS: The influences of defensin α1 at various concentrations on rat 1097 mesangial cell line cultured in vitro were evaluated with MTT assay.The different concentrations of U0126,signal-regulated protein kinase (MEK) inhibitor,were added into the culture mediums of mesangial cells to do blocking test.Incubated with a final concentration of 3 mg/L defensin α1,the phosphorylation of extracellular signal regulated kinase (ERK)1/2 and type IV collagen of mesangial cells in different times were evaluated by Western blotting.RESULTS: Defensin α1 at 3-20 mg/L enhanced proliferation of rat glomerular mesangial cells.The incubation times for the maximum effect on proliferation was 12 h (P<0.01),whereas defensin α1 concentration >20 mg/L decreased cell proliferation.The cell proliferation induced by defensin α1 was inhibited by U0126.Stimulation of the cells with defensin α1 at concentration of 3 mg/L for 5 minutes induced a maximum effect on a ratio of phosphorylation of ERK1/2 to total ERK.After 12 h incubation with defensin α1,an increase in type IV collagen was observed by Western blotting and continued to increase at 24 h and 48 h (P<0.01).CONCLUSION: Defensin α1 enhances rat glomerular mesangial cell proliferation and induces type IV collagen production by MAPK signaling pathway. 相似文献
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AIM:To study the role of ghrelin in cell protection by up-regulating heat shock protein 70 (HSP70) and inhibiting apoptosis induced by oxidative stress through extracellular regulated protein kinases 1/2 (ERK1/2) signaling pathway in the PC12 cells. METHODS:Sodium nitoprusside (SNP) was used to induce oxidative stress injury in the PC12 cells. The cultured PC12 cells were divided into SNP-injured group (incubated with SNP at 0.5 mmol/L for 6, 12, 18 and 24 h), ghrelin pretreatment group (ghrelin at 100 nmol/L was given 30 min before adding SNP); HSP70 inhibitor group (quercetin at 10 μmol/L was added 60 min before ghrelin treatment), ERK inhibitor group (ERK 1/2 inhibitor PD98059 was added 60 min before ghrelin treatment) and control group (added same amount of culture medium only). The apoptotic rate was detected by flow cytometry. The protein expression was determined by Western blot and immunocytochemistry. RESULTS:Compared with control group, the apoptotic rate of PC12 cells in SNP-injured group was significantly increased (P<0.05). Compared with SNP-injured group, ghrelin (100 nmol/L) pretreatment significantly inhibited SNP-induced apoptosis of PC12 cells (P<0.05), and significantly up-regulated the protein expression of HSP70 (P<0.05). Time-effect analysis showed that ghrelin had the most significant effect at 18 h after SNP injury. Quercetin, an inhibitor of HSP 70, significantly reduced the anti-apoptotic effect of ghrelin (P<0.05). Ghrelin pretreatment promoted the phosphorylation of ERK1/2. ERK1/2 inhibitor PD98059 significantly inhibited the effects of ghrelin on up-regulation of HSP70 expression (P<0.05). CONCLUSION:Ghrelin upregulates the expression of HSP70 and inhibits the apoptosis in the PC12 cells induced by oxidative stress by promoting the phosphorylation of ERK1/2. 相似文献
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AIM: To investigate the protective effect of astragaloside IV (ASIV) on angiotensin II (Ang II)- induced apoptosis of H9c2 cardiomyocytes. METHODS: H9c2 cardiomyocytes were treated with different concentrations of Ang II and ASIV. The effects of Ang II and ASIV on the viability of H9c2 cells was measured by CCK-8 assay. The optimum concentration of Ang II was 1 μmol/L and the concentrations of ASIV were 25, 50 and 100 μmol/L. The H9c2 cells was divided into 6 groups:control group, ASIV group, Ang II group, Ang II+ASIV (25 μmol/L) group, Ang II+ASIV 50 (μmol/L) group and Ang II+ASIV (100 μmol/L) group. The morphological changes of the H9c2 cells were observed under inverted phase-contrast microscope. Apoptosis was detected by TUNEL assay. The generation of reactive oxygen species (ROS) was detected by DCFH-DA staining. The protein expression of Bax, Bcl-2, nuclear factor E2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was determined by Western blot. H9c2 cardiomyocytes were transfected with negative control shRNA (NC) or Nrf2-shRNA (shRNA), and the cells were divided into 8 groups:NC+control group, NC+AngⅡgroup, NC+ASIV group, NC+AngⅡ+ASIV group, shRNA+control group, shRNA+AngⅡgroup, shRNA+ASIV group and shRNA+AngⅡ+ASIV group. ROS level was detected by ROS detection kit. The protein expression of Nrf2 and HO-1 was determined by Western blot. RESULTS: Ang II decreased the viability of H9c2 cells in a concentration-dependent manner (P<0.05). ASIV reversed the effect of Ang II on the viability of H9c2 cells in a concentration-dependent manner (P<0.05). Compared with control group, the apoptotic rate, the level of ROS and the protein expression of Bax in Ang II group were increased significantly, while the protein expression of Bcl-2, Nrf2 and HO-1 was decreased significantly (P<0.05). Compared with Ang II group, ASIV reversed the increase in apoptotic rate of H9c2 cells induced by Ang II in a concentration-dependent manner, reduced ROS level, down-regulated the protein expression of Bax and up-regulated the protein expression of Bcl-2, Nrf2 and HO-1 (P<0.05). After shRNA transfection, the effects of ASIV decreasing ROS production induced by Ang II and up-regulating the expression of Nrf2 and HO-1 were eliminated. CONCLUSION: ASIV protects H9c2 cardiomyocytes from apoptosis induced by Ang II, which may be related to reducing ROS generation and mediating the Nrf2/HO-1 signaling pathway. 相似文献
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AIM: To investigate the effect of ecdysterone (EDS) on H9c2 cardiomyocytes after oxidative stress. METHODS: H9c2 cells were cultured in vitro and divided into control group, high dose (2 μmol/L) of EDS group, middle dose (1.5 μmol/L) of EDS group, low dose (1 μmol/L) of EDS group, and H2O2 group. H9c2 cardiomyocytes in H2O2 group and high, middle and low doses of EDS groups were exposed to H2O2 for 6 h to establish the model of oxidative stress. The viability of the H9c2 cells was detected by CCK-8 assay. The apoptosis of H9c2 cells was analyzed by flow cytometry. The levels of lactate dehydogenase (LDH) and creatine kinase-MB (CK-MB) in the culture medium, and the levels of superoxide dismutase (SOD) and malondialdehyde (MDA) in the H9c2 cells were measured by colorimetry. The generation of reactive oxygen species (ROS) and the mitochondrial membrane potential were evaluated by flow cytometry and confocal laser scanning microscopy. The protein levels of Bax, Bcl-2 and cleaved caspase-3 in the H9c2 cells were determined by Western blot. RESULTS: Ecdysterone at the selected concentrations had no effect on the viability of H9c2 cells. Compared with control group, the levels of LDH, CK-MB, ROS and MDA, and the apoptotic rates of the H9c2 cells were significantly increased after treated with H2O2, but were decreased by EDS treatment in a dose-dependent manner. The levels of SOD and mitochondrial membrane potential of the H9c2 cells in H2O2 group were reduced significantly compared with control group, but high, middle and low doses of EDS treatments up-regulated the levels of SOD and mitochondrial membrane potential in H2O2-treated H9c2 cells. The protein levels of Bax and cleaved caspase-3 in the H9c2 cells in H2O2 group showed significant elevation in comparison with control group, and the protein expression of Bcl-2 declined in H2O2 group compared with control group, but high, middle and low doses of ecdysterone treatments down-regulated the protein levels of Bax, cleaved caspase-3 and up-regulated the expression of Bcl-2 in H2O2-treated H9c2 cells. CONCLUSION: Ecdysterone attenuates the effect of H2O2-induced oxidative stress on H9c2 cardiomyocytes. The mechanism may be involved in scavenging oxidative stress products, increasing antioxidant enzyme activity and improving mitochondrial function. 相似文献
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YU Fei TIAN Hua LU Shan GUO Ya-xin WANG Xiao-xu JIAO Peng ZONG Chuan-long YAO Shu-tong QIN Shu-cun 《园艺学报》2020,36(6):1006-1013
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LI Su-juan JIN Ke-ke ZHAO Ya-ping WANG Peng ZHAO Wen-xi GAO Kai-xuan YANG Wen-juan WANG Jia-lin WU De-ping 《园艺学报》2015,31(7):1259-1265
AIM: To explore the mechanisms of fluctuant high blood glucose-induced apoptosis of hepatocytes. METHODS: SD rats were randomly divided into normal control group (N), stable high blood glucose group (S), fluctuant high blood glucose group (F) and insulin group (I). Diabetic rats were induced by intraperitoneal injection of streptozotocin (65 mg/kg), and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of ordinary insulin and glucose at different time points every day. The blood glucose fluctuation patterns of the animals in F group within 12 weeks were similar every day and no significant difference of the HbA1c concentration was observed compared with S group, indicating that the fluctuant hyperglycemia was successfully established in F group. The activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the content of malondialdehyde (MDA) and nitric oxide (NO) in the homogenate of the liver tissues were detected by colorimetry. The mRNA and protein levels of JNK, p-JNK, Bax and Bcl-2 were examined by RT-PCR and Western blot. RESULTS: After 12 weeks, the increases in the intakes of food and water, the urine output, and the abnormal liver function were observed in S group, I group and F group. Compared with N group, the MDA level was increased, the content of NO and the activity of SOD and GSH-Px were decreased, and up-regulation of JNK mRNA and p-JNK and Bax proteins, and down-regulation of Bcl-2 were also found in S group, I group and F group. The above effects were more obviously showed in F group. CONCLUSION: Oxidative stress activates JNK-MAPK signaling pathway, which is involved in fluctuant high glucose-induced apoptosis of hepatocytes. 相似文献
19.
WANG Yu-lin LV Lin-lin WANG Xia GAO Yong-qing ZHOU Zhao LIU Ge-xiu WANG Lin-jing 《园艺学报》2018,34(6):975-981
AIM: To study the effect of Lycium barbarum polysaccharides (LBP) on oxidative stress injury of human endothelium-like EA.hy926 cells induced by hydrogen peroxide (H2O2). METHODS: The EA.hy926 cell model of oxidative stress injury was established by H2O2 treatment. The EA.hy926 cells were divided into 5 groups:control group, damage (H2O2 at 50 mmol/L) group, LBP (100 mg/L) group, anti-damage groups (LBP at 50 mg/L, 100 mg/L or 200 mg/L+50 mol/L H2O2), and LY294002 (20 μmol/L) group. The effect of LBP at different concentrations on the cell viability of EA.hy926 cells was measured by CCK-8 assay, and the optimum concentration of LBP was screened out. The apoptotic of EA.hy926 cells was analyzed by flow cytometry. Acridine orange/ethidium bromide (AO/EB) staining was used to observe the morphological characteristics of the apoptotic cells. The cell migration ability was detected by scratch method. The levels of nitric oxide (NO) and vascular endothelial growth factor (VEGF) in the cell culture medium were examined. The protein levels of cleaved caspase-3, Bax, Bcl-2, endothelial NO synthase (eNOS), p-eNOS and p-Akt were determined by Western blot. RESULTS: LBP at concentration of 100 mg/L significantly attenuated the injury of EA.hy926 cells induced by H2O2, as indicated by improved cell viability (P<0.05) and decreased apoptosis (P<0.05). Pretreatment with LBP elevated the levels of NO and VEGF (P<0.05), and promoted the migration ability of EA.hy926 cells. LBP also increased the Bcl-2/Bax ratio, down-regulated the protein level of cleaved caspase-3, and up-regulated the protein levels of eNOS and p-eNOS. The protective effect of LBP were abolished by pretreatment of the EA.hy926 cells with the inhibitor of PI3K (P<0.05). As a result, the protein level of p-Akt was down-regulated, and the level of NO was also significantly reduced. CONCLUSION: LBP has protective effect on H2O2 -induced EA.hy926 cells by attenuating apoptosis of the cells. The mechanism is closely related to the activation of PI3K/Akt/eNOS signaling pathway. 相似文献
20.
AIM: To explore whether morphine protects oxidative stress-damaged myocardial cells by inhibiting the PERK pathway to reduce endoplasmic reticulum stress and prevent mitochondrial permeability transition pore (mPTP) opening. METHODS: Rat myocardial H9c2 cells were cultured to establish an oxidative stress model, and then randomly divided into control group, H2O2 group, H2O2+morphine group, H2O2+morphine+PERK pathway inhibitor GSK2656157 group, morphine group and GSK2656157 group. Immunohistochemical method was used to detect the effects of morphine on expression of glucose-regulated protein (GRP) 78 and GRP94 induced by oxidative stress. The protein levels of PERK signaling pathway-related molecules were determined by Western blot. Confocal microscopy was used to observe the effects of morphine on mPTP opening and endoplasmic reticulum induced by oxidative stress. Cellular toxicity was detected by lactate dehydrogenase (LDH) kit and cell viability was measured by MTT assay. RESULTS: Compared with control group, GRP78 and GRP94 proteins in H2O2 group were strongly expressed, and the brown-yellow particles were significantly increased, but morphine significantly inhibited this process. Compared with control group, the phosphorylation of PERK was significantly reduced with GSK2656157 treatment at different concentrations, among which 2 μmol/L had the most significant effect (P < 0.05). Oxidative stress significantly increased the protein levels of GRP78, GRP94, p-PERK and CHOP, but significantly decreased p-GSK-3β level. These changes were inhibited by morphine, and the effects of morphine were further enhanced by GSK2656157 (P < 0.05). Compared with control group, oxidative stress significantly reduced the fluorescence intensity of mitochondrial TMRE and ER-Tracker Red. Morphine significantly inhibited this effect even when mitochondrial membrane potential was reduced, mPTP was open, and endoplasmic reticulum was damaged, while GSK2656157 further enhanced the effect of morphine (P < 0.05). Compared with control group, H2O2 significantly increased cellular toxicity and decreased the cell viability. Morphine inhibited this effect and GSK2656157 significantly enhanced the effect of morphine (P < 0.05). CONCLUSION: Morphine protects cardiac H9c2 cells under oxidative condition by inhibiting endoplasmic reticulum stress through PERK pathway and preventing the mPTP opening via GSK-3β inactivation. 相似文献