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H9c2 myocardial cells to establish the purpose of training the oxidative stress model, select and choice of ERK1 / 2 pathway as an object of study, specific inhibitor U0126 ERK1 / 2 pathway to further explore the possible mechanism of action, observation of resveratrol on myocardial cells resistant oxidative stress protection and mechanism of injury. By passage cultured H9c2 cells. The experiment is divided into the following five groups: normal control group, hydrogen peroxide (H202) group, resveratrol H2O2 group, resveratrol UO126 H2O2 group, UO126 H2O2 group. H9c2 myocardial cell morphology changes observed under an inverted phase contrast microscope, after the end of the experiment, the release of lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity, thiobarbituric acid colorimetric method determination content of malondialdehyde (MDA), the use of flow cytometry to detect myocardial cell apoptosis. ERK1 / 2 protein expression was determined by Western-blot. Results 1.1.H2O2 group compared with the control group of LDH activity significantly with the increase (998.08 ± 23.07 vs 477.11 ± 17.78, (P <0.05)) of MDA activity significantly increase (32.05 ± 1.76 vs 7.42 ± 1.51, P lt; 0.05), the activity of SOD significantly with reducing (15.43 4.52vs 35.03 ± 2.17, P <0.05), were compared between the two groups the difference was statistically significant. 2. Resveratrol H2O2 group than in the H2O2 group, LDH activity was significantly decreased (617.3 ± 11.23 vs 998.08 ± 23.07, P lt; 0.05), MDA activity also significantly lower (16.33 ± 1.68 vs 32.05 ± 1.76, P <0.05), SOD activity was significantly increased (29.03 3.18 vs 15.43 4.52, P lt; 0.05), the two groups were compared statistically significant difference. Apoptosis rate, the blank control cell growth, apoptosis rate is a low 6.73 ± 2.38. The H202 group a large number of apoptotic cells, apoptosis was 56.2 ± 4.73, the difference was statistically significant (P lt; 0.05) compared with the blank control group; resveratrol H202 group apoptosis rate significantly decreased 38.17 3.08 , compared with the H202 group difference was statistically significant (P lt; 0.05). 4. UO126 H2O2 group comparison control group LDH activity significantly with reducing (658.19 ± 21.38 vs 998.08 ± 23.07, P lt; 0.05) of MDA activity also significantly reduce (20.01 ± 3.16 vs 32.05 ± 1.76, P <0.05), the activity of SOD significantly with increased (22.33 ± 1.78 vs 15.43 ± 4.52, P <0.05), were compared between the two groups the difference was statistically significant. Resveratrol UO126 H2O2 with UO126 H2O2 group of LDH, MDA and SOD activity in comparison, there was no significant difference. 5.H2O2 significant upregulation of ERK1 / 2 expression, resveratrol H202 group significantly lowered H202-induced ERK1 / 2 expression, these differences were statistically significant; and UO126 H2O2 resveratrol group and resveratrol alcohol H202 group, ERK1 / 2 expression differences. Conclusion 1.H2O2 H9c2 cells can be induced oxidation occurs, and cell apoptosis; resveratrol can antagonize H202 H9c2 myocardial cells caused by oxidation, inhibition of H202 induced H9c2 myocardial apoptosis of H9c2 The protective effect of myocardial cells; resveratrol play The H9c2 cells protective effect may be achieved through the ERK1 / 2 pathway.
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