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1.
AIM: To investigated the role of CT-1 in the hypertensive ventricular remodeling. METHODS: The cardiac fibroblasts in 3-4 passages were cultured in vitro, and divided into eight groups according to the different intervention factors: group C (control); group DM: dimethyl sulphoxide (DMSO); group P: cultured under high hydrostatic pressure (160 mmHg); group ASODN: interfered with CT-1 antisense oligodeoxynucleotides (10 μmol/L); group SODN: incubated with CT-1 sense oligodeoxynucleotides (10 μmol/L); group AG: interfered with AG490 (25 μmol/L); group PD: interfered with PD98059 (20 μmol/L); group LY: interfered with LY 294002 (10 μmol/L). Western blotting was employed to assess the expression of STAT3, ERK1/2 and PI3-K respectively at protein level. Cell proliferation was quantified by MTT. RESULTS: High hydrostatic pressure stimulated the proliferation of cardiac fibroblasts, upregulated the expression of CT-1. CT-1ASODN inhibited the proliferation of cardiac fibroblasts (0.132±0.013 vs 0.154±0.011, P<0.05). ASODN extensively inhibited the expression of STAT3, ERK1/2 and PI3-k respectively at protein level (2.09±0.25 vs 2.47±0.28, P<0.05), (1.13±0.19 vs 1.61±0.22, P<0.05), (1.25±0.23 vs1.71±0.25, P<0.05). AG490, a JAK-STAT3 inhibitor, reversed the increase in the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure and the expression of ERK1 phosphorylation (0.118±0.018 vs 0.155±0.010, P<0.05). PD98059, a MAPK-ERK1/2 inhibitor, increased the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.185±0.011 vs 0.155±0.010, P<0.05) and the expression of STAT3 phosphorylation (1.83±0.23 vs 1.58±0.22, P<0.05). LY294002, a PI3-K inhibitor, had no effect on the proliferation of cardiac fibroblasts stimulated by high hydrostatic pressure (0.157±0.015 vs 0.155±0.010, P>0.05). No difference of the expression of the above factors was observed in SOND (0.151±0.010 vs 0.154±0.011, P>0.05) and DMSO (0.141±0.017 vs 0.155±0.010, P>0.05) groups as compared with the control group. CONCLUSION: Under high hydrostatic pressure, the proliferation of cardiac fibroblasts is essentially mediated by STAT3, independent of PI3-K and the action is negatively regulated by ERK1/2 via inhibiting STAT3.The interaction between STAT3 and ERK1/2 may assist CT-1 in developing adequate cardiac fibroblast proliferation.  相似文献   

2.
AIM: To investigate the effect of growth arrest-specific protein 6(Gas 6) on H9c2 cell apoptosis induced by anoxia-reoxygenation (A/R) and its possible relationship with PI3K/Akt pathway. METHODS: Cultured H9c2 cell line of cardiomyocytes was randomly divided into 4 groups: normal control group, anoxia-reoxygenation group (A/R), anoxia-reoxygenation+Gas6 group (A/R+Gas6) and anoxia/reoxygenation+Gas6+LY294002 group (A/R+Gas6+LY294002). The procedure of A/R was performed in cultured H9c2 cells by 3 h of anoxia and then 3 h of reoxygenation. The viability of the cells and the activity of caspase-3 were detected by automatic biochemistry analytic instrument. Cell apoptotic rates were evaluated by flow cytometry. The protein level of phosphorylated Akt(p-Akt) was determined by Western blotting. RESULTS: Compared with control group, the cell viability was significantly decreased, and caspase-3 activity, cell apoptotic rate and the protein level of p-Akt were increased in A/R group. Compared with A/R group, the caspase-3 activity and cell apoptotic rate reduced markedly, while the cell viability and the protein level of p-Akt were significantly increased in A/R+Gas6 group .The effect of Gas6 was inhibited by LY294002. CONCLUSION: Gas6 may protect the H9c2 cells from anoxia-reoxygenation-induced apoptosis. Its mechanism is possibly involved in the activation of PI3K/Akt survival pathway via increasing the phosphorylation of Akt protein.  相似文献   

3.
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   

4.
AIM:To investigate the characteristics of pathological injury and its relationship with the transformation of energy metabolism of hypertrophic cardiomyocytes after hypoxia-reoxygenation. METHODS:Cultured rat cardiomyocytes were induced to be hypertrophy by angiotensin Ⅱ (Ang Ⅱ) and norepinephrine (NE). Glucose oxidation rate (GOR), glucolysis rate (GLR) and fatty acid oxidation rate (FOR) were determined by liquid scintillation counting, and cell apoptosis was detected by TUNEL. RESULTS:(1) Compared with the normal cardiomyocytes (NC), the GOR and GLR were slightly higher and the FOR was slightly lower in the group of hypertrophic cardiac cells (HC) than that in the group of normal cardiomyocytes cultured under the normal oxygen partial pressure. The apoptosis rate had no difference between the two groups. (2) The apoptosis rate of hypertrophic cardiomyocytes after hypoxia was significantly higher than that of hypertrophic cardiomyocytes in normal culture. It was higher and moreover, some necrosis cardiomyocytes appeared after reoxygenation. (3) GOR and FOR in both group (NC and HC) were slightly lower in a time-dependent manner after hypoxia than that in each group in normal culture condition. GLR had no difference in both group. The GOR was more lower in both NC and HC group when reoxygenation than that at the point of hypoxia for 2 hours, but the GLR and FOR were significantly higher in HC than that in NC when reoxygenation. (4) The GOR was significantly higher and the GLR and FOR were significantly lower in the hypertrophic cardiomyocytes group (HC) with dichloroacetate (DCA, 1 000 μmol/L) or trimetazidine (TMZ, 1 μmol/L) treated respectively than that in the responded hypertrophic cardiomyocytes after stimulation by hypoxia-reoxygenation. In the meanwhile, the apoptosis rate also was markedly lower in the treated hypertrophic cardiomyocytes group. CONCLUSION:The transformation of energetic metabolism pathway plays an important role in the pathogenesis (mainly the apoptosis) of the hypertrophic cardiomyocytes after hypoxia-reoxygenation.  相似文献   

5.
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6.
《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   

7.
AIM: To investigate the protective effects of puerarin (PUE) pretreatment on hypoxia/reoxygenation (H/R) injury in human umbilical vein endothelial cells (HUVECs), as well as its possible mechanism and the signal transduction pathways involved. METHODS: HUVECs were randomly divided into normal control group, H/R group, PUE pretreatment group and PUE+H/R group (1.0×10-3 mol/L, PUE pretreated the cells for 24 h before H/R). The protein expression of endothelial nitric oxide synthase (eNOS) was measured by Western blot. The activity of constitutive NOS (cNOS) was determined via chemical colorimetric methods. Apoptosis of HUVECs was detected by TUNEL assay. In addition, the cells were treated with ERK inhibitor U0126 (1.0×10-5 mol/L) or PKB/Akt inhibitor LY294002 (5.0×10-5 mol/L) for 1 h before PUE pretreatment, and then H/R was performed.RESULTS: Compared with control group, H/R decreased the protein expression of eNOS (P<0.05), and PUE pretreatment up-regulated it (P<0.05). This effect of PUE was inhibited by U0126 or LY294002 (P<0.05). Compared with control group, the activity of cNOS decreased in H/R group (P<0.05), while it increased after PUE pretreatment (P<0.05). Compared with control group, the apoptotic index significantly increased in H/R group (P<0.01). PUE pretreatment reduced the apoptotic index (P<0.01). CONCLUSION: H/R decreases the protein expression and enzyme activity of eNOS in HUVECs, and induces apoptosis of HUVECs. PUE pretreatment up-regulates the protein expression and enzyme activity of eNOS, and reduces the apoptosis of HUVECs with H/R injury. The protective effect of PUE might be through increasing eNOS protein expression via ERK1/2 and PKB/Akt signaling pathways.  相似文献   

8.
AIM: To explore the potential mechanism of microRNA-30a (miR-30a) overexpression in neonatal rat cardiomyocytes during hypoxia/reoxygenation (H/R). METHODS: The miR-30a overexpression was induced in primary neonatal rat cardiomyocytes by lentivirus transfection. The cardiomyocytes were divided into 5 groups: normal group, H/R group, LV-GFP+H/R group, LV-GFP-miR-30a+H/R group and 3-methyladenine(3-MA)+H/R group. The expression level of miR-30a after lentivirus transfection and H/R was determined by real-time PCR, while the protein levels of LC3 and Beclin-1 after H/R and lentivirus transfection were detected by Western blotting. The cardiomyocyte death after H/R were measured by TUNEL and PI staining. RESULTS: Compared with LV-GFP group, significant down-regulation of Beclin-1 protein level was observed in cardiomyocytes with miR-30a overexpression, while the protein levels of Beclin-1 and LC3 in the cardiomyocytes with miR-30a overexpression were down-regulated after H/R, and apoptosis of these cells were significantly decreased after H/R. CONCLUSION: The protein level of Beclin-1 is down-regulated in cardiomyocytes with miR-30a overexpression. Inhibition of autophagy decreases the cardiomyocyte death after H/R.  相似文献   

9.
AIM: To observe the effect of glycine liposomes on the mitochondrial membrane potential and the apoptosis rate in cardiomyocytes induced by hypoxia/reoxygenation injury. METHODS: A cardiomyocyte injury model was established by using hypoxia/reoxygenation. DiOC6(3) as fluorescence molecular probe was used to detect the mitochondrial membrane potential in each group. The method of Annexin V associated with PI was used to detect the apoptosis ratio in each group. RESULTS: (1) The result of flow cytometry showed that the mitochondrial membrane potential of cardiomyocytes in H/R group was obviously lower than that in control group (P<0.01). The decrease in mitochondrial membrane potential in Gly-liposome group was the lowest, the percentage of cells about the part of hypofluorescence was (9.61±0.76)%, which was lower than that in glycine group (P<0.01). (2) The apoptosis rate of cardiomyocytes in H/R group was higher than that in control group (20.78±1.58)%,P<0.01. After the treatment of Gly-liposome, the apoptosis rate of cardiomyocytes was lower than that in glycine group (P<0.01). No difference in the apoptosis ratios between blank-liposome group and H/R group was observed(P>0.05).CONCLUSION: Glycine liposomes protect cultured cardiomyocytes against hypoxia/reoxygenation injury. Glycine liposomes produce the better protective effects than glycine.  相似文献   

10.
AIM: To investigate the role of PI3K-IP3R-Ca2+ pathways in cardiomyocyte hypertrophy induced by tumor necrosis factor-α (TNF-α). METHODS: Myocardial cells of neonatal rats were cultured in vitro. The hypertrophic model was induced by TNF-α. The protein content was assayed with Lowry's method. The volumes of the cardiomyocytes were detected by computer photograph analysis system. The protein synthesis was determined by the method of[3H]-leucine incorporation.[Ca2+]i transient was measured by Till image system with cell-loading Fura-2/AM. RESULTS: LY294002, a PI3K inhibitor, significantly suppressed the amplitude elevation of the spontaneous[Ca2+]i transients induced by TNF-α in cultured ventricular myocytes from neonatal rats. The effect was similar to that of LY294002+2-APB (P>0.05), but lower than that in LY294002+ryanodine group (P<0.05). LY294002 significantly reduced the enhancements of protein content,[3H]-leucine incorporation and cell size induced by TNF-α. The effect was similar to that in 2-APB+LY294002 group, but higher than that in 2-APB group and lower than that in ryanodine+LY294002 group. CONCLUSION: TNF-α induces cardiac hypertrophy through PI3K-IP3R-Ca2+ pathways.  相似文献   

11.
AIM: To explore the effects of p38 mitogen-activated protein kinases (MAPK) and phosphoinositide 3-kinases (PI3K)/Akt on interleukin (IL)-6, the endothelin (ET)-1-mediated process of airway fibroblast activation induced by injured human bronchial epithelial cells (HBE). METHODS: Human primary cultured airway fibroblasts were co-cultured with HBE pre-treated with or without poly-L-arginine (PLA). The procedure was also performed in the presence or absence of p38 MAPK selective inhibitor SB203580, PI3K selective inhibitor LY294002 or ETA receptor blocker BQ123, respectively. Immunostaining, Western blotting or ELISA were used for detecting α-smooth muscle actin (α-SMA) expression, the activities of p38 MAPK and Akt in fibroblasts or IL-6 levels in supernatants of fibroblasts. In addition, fibroblasts were mixed with soluble collagen and cultured with HBE treated as the same mentioned above, the gel contraction was measured by serial area measurements. RESULTS: ET-1 and IL-6 levels ［(13.69±1.36) ng/L, (56.7±10.7) ng/L］ in the supernatants of fibroblasts cultured with injured HBE were significantly higher than those in the supernatants of fibroblasts cultured with HBE ［(3.79±0.64) ng/L, (15.5±3.2) ng/L］. BQ123, SB203580 or LY294002 decreased IL-6 levels ［(27.2±3.1) ng/L, (31.5±3.6) ng/L, (41.3±3.2) ng/L］ differently in the supernatants of fibroblasts induced by injured HBE. Activation of p38 MAPK preceded Akt in fibroblasts cultured with injured HBE. BQ123 reduced the phosphorylation levels of p38 MAPK and Akt. SB203580 concentration-dependently attenuated Akt phosphorylation, while LY294002 had little effect on p38 MAPK phosphorylation. Fibroblasts expressed more α-SMA after cultured with injured HBE and showed significant increase in the gel contraction compared to fibroblasts cultured with HBE ［percentage of gel contraction: (61.2±2.7)% vs (15.4±7.3)%］, all these effects were diminished or inhibited by BQ123, SB203580 or LY294002. Furthermore, the effects of BQ123 and SB203580 on decreased gel contraction were stronger than the effect of LY294002. CONCLUSION: ET-1 exerts a key role in the airway fibroblasts activation induced by injured HBE through activating p38 MAPK, PI3K/Akt signaling and promoting IL-6 expression.  相似文献   

12.
AIM: To investigate whether the protection mechanism of Fuzi polysaccharide (FPS) is related to inhibition of endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes with hypoxia/reoxygenation (H/R). METHODS: Cultured rat myocardial cells were divided into control group, H/R group (hypoxia for 3 h and reoxygenation for 6 h) and different concentrations of FPS (0.1 g/L, 1 g/L, 10 g/L or 20 g/L) +H/R groups. The cell survival was detected by MTT assay and cell apoptosis of cardiomyocytes was measured by flow cytometry using Annexin V-FITC staining. The expression of glucose-regulated protein 78 (GRP78), CCAAT/enhancer-binding protein homologous protein (CHOP) and caspase-12 were determined by Western blotting. The mRNA expression of CHOP and caspase-12 was detected by quantitative PCR. RESULTS: After reoxygenation, the expression of GRP78, CHOP and caspase-12 in cardiomyocytes was increased. Compared with H/R group, the expression of GRP78, CHOP and caspase-12 in FPS+H/R groups was significantly inhibited, the survival rate of cardiomyocytes was increased and the apoptosis of cardiomyocytes was inhibited. This protective effect of FPS was in a dose-dependent manner and reached its peak at 10 g/L. CONCLUSION: Fuzi polysaccharide protects cardiomyocytes from H/R injury. The mechanism is related to inhibiting endoplasmic reticulum stress.  相似文献   

13.
AIM: To observe the role of peroxysome proliferator activated receptor-γ (PPAR-γ) and the relationship of cyclooxygenase-2 (COX-2) and PPAR-γ in injury of cultured rat cortical neurons induced by hypoxia/reoxygenation. METHODS: Primary rat cortical neurons were cultured. Experiments include control group, hypoxia/ reoxygenation group and hypoxia/ reoxygenation with PPAR-γ agonist group. Cell viability was surveyed by MTT assay. COX-2 protein expression was measured by Western blotting.RESULTS: Neuron viability raised dramatically in hypoxia/reoxygenation with PPAR-γ agonist group, compared with hypoxia/reoxygenation group (P<0.05). The COX-2 protein expression in hypoxia/ reoxygenation with PPAR-γ agonist group decreased significantly compared with hypoxia/ reoxygenation group (P<0.05). CONCLUSION: PPAR-γ agonist inhibits the expression of COX-2 and reduces obviously cortical neuron injury induced by hypoxia/ reoxygenation. It may protect cortical neurons by down-regulating the expression of COX-2.  相似文献   

14.
AIM: To investigate the protective effect of hypoxic preconditioning on human bone marrow mesenchymal stem cells (hBM-MSCs), and to provide basic experimental support for more effective autologous stem cell transplantation in aged patients. METHODS: The old hBM-MSCs were subjected to hypoxic preconditioning using a hypoxia incubator chamber for 24 h. The cells were divided into young group, old group and old+hypoxia group (with 24 h hypoxic preconditioning). Hydrogen peroxide (H2O2, 300 μmol/L) was applied to simulate the oxidative stress. The cells were treated with 50 μmol/L LY294002 for 2 h to inhibit PI3K/AKT pathway. BrdU incorporation and CCK-8 assay were used for analyzing the cell proliferation and viability. The protein levels of Bax, Bcl-2 and p-AKT were measured by Western blot. RESULTS: BrdU-positive cells, which represented the cell proliferation, and the cell viability were significantly increased in old+hypoxia group compared with old group (P<0.05). The protein level of Bax decreased (P<0.05) and Bcl-2 increased (P<0.05) in old+hypoxia group compared with old group after using 300 μmol/L H2O2 simulate. the oxidative stress. The phosphorylation of AKT was enhanced by hypoxic preconditioning in old group (P<0.05). The protective effect of hypoxic preconditioning on the cell survival was decreased after treated with LY294002 (inhibitor of the PI3K/AKT pathway) (P<0.05). CONCLUSION: Hypoxic preconditioning increases the survival and proliferation of old hBM-MSCs by activation of AKT pathway.  相似文献   

15.
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   

16.
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   

17.
AIM: To prepare glycine liposome microparticle and observe the effect of glycine liposomes on cardiomyocyte injury induced by hypoxia/reoxygenation. METHODS: （1） Reverse-phase evaporation method was used to produce glycine liposomes, the effects of different organic solvents: aether, chloroform and two mixtures of aether/chloroform on entrapment efficiency were evaluated, transmission electron microscope was used to detect the particle diameter of glycine liposomes. （2） A cardiomyocyte injury model was established by using hypoxia/reoxygenation, the activities of lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase isoenzyme (CK-MB) of each group were detected. RESULTS: The entrapment efficiency of glycine liposomes prepared with the mixtures of aether/chloroform is highest compared with other organic solvents （64.8％, P<0.01）; all of glycine, glycine liposomes and blank liposomes inhibited the release of LDH, CK and CK-MB induced by hypoxia/reoxygenation in cultured cardiomyocytes, and the inhibition by glycine liposomes was the most obvious （P<0.05，P<0.01）. CONCLUSIONS: The mixtures of aether/chloroform can be used to prepare glycine liposomes, which can get higher entrapment efficiency; glycine liposomes protects cultured cardiomyocytes against hypoxia/reoxygenation-induced injury, and the protective effect of glycine liposomes is better than that of glycine.  相似文献   

18.
AIM: To study the role of hypoxia preconditioning (HP) in hypoxia-reoxygenation (HR)-induced apoptosis in neonatal rat cardiomyocytes and the possible mechanisms. METHODS: Cultured neonatal rat cardiomyocytes were divided into three groups: normal group, HP+H/R group and H/R group. Acridine orange (AO) staining was performed to detect morphological changes of apoptotic cells. Apoptosis rates of cardiomyocytes were detected by flow cytometry. Colorimetric assay was used to detect caspase-3 activity. Expression of Bcl-2 protein was detected by immunohistochemistry combined with computer image analysis. RESULTS: Apoptotic cells were detected by AO staining after hypoxia of 6 h followed by 3 h-reoxygenation. The hypodiploid apoptotic peak was detected by flow cytometry with the apoptotic rates of (29.7±5.4)%. A significantly reduced apoptotic rates of (7.8±1.3)% was detected in HP group（P＜0.01）. The caspase-3 relative activity of cardiomyocytes induced by H/R was 5.9±0.8, significantly higher than that of control group. HP markedly reduced caspase-3 relative activity to 2.6±0.5 in contrast with H/R group （P＜0.01）. Bcl-2 protein was positive in normal cardiomyocytes with an A value of 119.4±7.1. The A value of H/R group was 99.6±5.0, significantly lower than that in normal group （P＜0.01）. The A value of HP+H/R group was 126.5±6.2, significantly higher than that in H/R group（P＜0.01）. CONCLUSION: HP inhibits H/R-induced apoptosis of cardiomyocytes by improving the expression of Bcl-2 and reducing caspase-3 activity.  相似文献   

19.
AIM: To examine the effects of high glucose (HG) on the expression of Snail1 and protein kinase B (Akt)/glycogen synthase kinase 3β (GSK-3β) in primary renal tubular epithelial cells (RTECs). METHODS: The primary RTECs were randomly treated with normal glucose, high glucose or D-mannitol for 30 min~72 h. RT-PCR and Western blotting were used to observe the expression of Snail1, Akt and GSK-3β at mRNA and protein levels in these cells. The primary cultured RTECs were pretreated with LY294002 (a PI3K inhibitor, 25 μmol/L) to observe the specific inhibitory effects of phosphatidylinositol 3-kinase (PI3K) on HG-induced expression of Snail1 protein. RESULTS: Treatment of RTECs with HG resulted in increased mRNA and protein levels of Snail1, Akt1, and phosphorylation of Akt and GSK-3β. LY294002 blocked the HG-induced up-regulation of p-Akt, p-GSK-3β and Snail1 expression at protein level, but no effect of LY294002 was seen on the total protein expression of Akt1 and GSK-3β. HG did not affect the expression of GSK-3β at mRNA and protein levels. CONCLUSION: HG-induced up-regulation of Snail1 may be regulated by Akt/GSK-3β pathway in RTECs.  相似文献   

20.
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   

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