蜂胶对乳鼠心肌细胞氧化损伤的保护作用

目的:探讨蜂胶(propolis)对乳鼠心肌细胞氧化损伤的作用及其可能机制。方法:建立乳鼠心肌细胞过氧化氢(H2O2)损伤模型,通过观察细胞形态及细胞存活率,检测培养液中乳酸脱氢酶(LDH)活性、超氧化物歧化酶(SOD)活性及脂质过氧化产物丙二醛(MDA)的含量,观察不同浓度蜂胶(50、100、200 mg/L)对乳鼠心肌细胞氧化损伤的影响。结果:不同浓度的H2O2(50、100、200、400、800μmol/L)孵育乳鼠心肌细胞4 h后,心肌细胞存活率随H2O2浓度增加而降低,呈剂量依赖性;细胞形态出现明显损伤改变,心肌细胞伪足回缩、体积变小、自律搏动减弱。与模型组比较,经蜂胶预处理心肌细胞培养上清液中LDH释放量、MDA生成量降低,SOD活性提高;细胞存活率显著改善,差异有统计学意义(P<0.05)。结论:蜂胶对H2O2所致的乳鼠心肌细胞氧化损伤有明显的保护作用,其机制可能是通过抑制脂质过氧化,增强心肌细胞膜抗氧化能力所致,至于其确切机制有待进一步探讨。

Protective effects of propolis on the hydrogen peroxide.injured myocardial cells in neonate rats

Objective ：To investigate the protective effects and potential mechanisms of propolis on hydroperoxide-induced myocardial injury in neonate rats. Methods ： Hydrogen peroxide （ H2O2 ） induced myocardial injury models were established in neonate rats. The protective effects of propolis administered in different dosage（50,100,200 mg/L） were determined through observing the cellular morphology and viability of the oxidatively injured myocardial cells,and examining the activity of lactate dehydrogenase （ LDH ） and superoxide dismutase （ SOD ） as well as the level of malondialdehyde （ MDA ）. Results：Different concentrations of I42 02 （50,100,200,400,800 μmol/L） were incubated in the eardiomyoeytes from neonate rats for 4h neonatal rat, and the findings showed that myocardial cell viability was decreased with increased concentration of H2O2 , which indicated a dose - dependent fashion. Also, the cell morphology was significantly damaged, with retracted pseudopodia and shrunk size of the myocardial cells, and weakened automatic impulse of the myocardium. As compared with the model group, the myocardial cell culture treated with propolis indicated significantly decreased contents of LDH and MDA, yet notably increased SOD activity and improved cellular viability. The difference was significant （ P 〈 0.05 ）. Conclusion ： Propolis can evidently have protective effects on the injured myocardial cells from oxidation induced by H2O2. The potential mechanisms may be associated with the checked lipid peroxidation but enhanced antioxidant capacity of the myocardial cell membrane,yet the exact mechanism remains to be further determined.