银杏达莫注射液对缺氧缺糖损伤大鼠心肌细胞的保护作用

Protection of Ginkgo-Diyidamolum Injection on Rat Myocardial Cells Injured by Oxygen-Glucose Deprivation

目的探讨银杏达莫注射液对大鼠心肌细胞缺氧缺糖损伤的保护作用。方法建立乳鼠心肌细胞缺氧缺糖损伤模型。将培养的细胞随机分成5组:正常组、缺氧缺糖组、银杏达莫注射液低、中、高剂量组(0.28、0.84、1.40 mg·mL^(-1))。观察银杏达莫注射液对心肌细胞一氧化氮(NO),丙二醛(MDA),乳酸脱氢酶(LDH)含量和超氧化歧化酶(SOD)活性的影响,采用流式细胞仪技术检测各组细胞的凋亡率,采用逆转录-聚合酶链反应(RT-PCR)技术监测各组对心肌细胞缝隙连接蛋白43(Cx43)基因转录水平的影响。结果相对于缺氧缺糖组,银杏达莫注射液明显抑制NO、MDA、LDH的产生,更能显著增强胞内SOD活性。银杏达莫注射液中、高剂量组可明显改善心肌细胞形态,抑制细胞凋亡,有效下调心肌细胞中Cx43基因的过表达。结论银杏达莫注射液对大鼠心肌细胞的缺氧缺糖损伤有明显的保护作用,其作用机制与抗氧化、抑制细胞凋亡及维持心肌缝隙连接通道等相关。

OBJECTIVE To explore the protective effect of ginkgo-diyidamolum injection on rat myocardial cells injured by oxy- gen-glucose deprivation. METHODS The model of oxygen-glucose deprivation in rat myocardial cells was established. The cells were randomly divided into five groups： normal group, oxygen-glucose deprivation group, different ginkgo-diyidamolum injection dosage groups（0. 28, 0. 84, 1.40 mg · mL-1 ）. The effects of ginkgo-diyidamolum injection on NO level, malondialdehyde （MDA） level, changes in the concentrations of lactate dehydrogenase （LDH）, superoxide dismutase （SOD） activity were evaluated. Cells apoptosis rate was determined by flow eytometry. The gene transcription level of myocardial cell gap junction protein 43 （ Cx43 ） was monitored by RT-PCR. RESULTS Compared with oxygen-glucose deprivation group, ginkgo-diyidamolum injection could reduce the content of intracellular NO, MDA, LDH and enhance the activity of SOD. Ginkgo-diyidamolum injection high dose and middle dose groups obvi- ously improved the myocardial cell morphology, inhibited cell apoptosis and Cx43 gene in myocardial cells. CONCLUSION Ginkgo- diyidamolum injection has a strong protective effect when myocardial cells injured by oxygen-glucose deprivation, which is related to the antioxidant effect, inhibition of cell apoptosis, and maintaining the role of myocardial gap junction channel.