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目的:以金属硫蛋白为着眼点,探讨附子多糖对缺氧复氧后心肌细胞的保护机制。方法:建立乳鼠心肌细胞缺氧/复氧模型,将乳鼠心肌细胞分为正常对照组、缺氧/复氧组、附子多糖组。缺氧/复氧组给予心肌细胞缺氧3 h后复氧6 h;附子多糖组分别给予10.0,1.0,0.1 g.L-1的附子多糖预处理心肌细胞24 h后再予缺氧3 h后复氧6 h。ELISA检测金属硫蛋白的含量,流式细胞仪检测细胞的凋亡率,测定心肌细胞内丙二醛(MDA)的含量和细胞培养液中乳酸脱氢酶(LDH)的含量。结果:与缺氧/复氧组相比较,附子多糖可以呈剂量依赖形式地增加金属硫蛋白的合成,减少MDA的生成与LDH的的释放,抑制心肌细胞凋亡,在10.0 g.L-1时作用达到峰值。结论:附子多糖对于缺氧复氧心肌细胞损伤具有保护效应,其机制与附子多糖促进金属硫蛋白的合成,对抗氧化应激损伤,抑制心肌细胞凋亡有关。
OBJECTIVE: To investigate the protective mechanism of monkshood polysaccharide on cardiomyocytes after hypoxia and reoxygenation with the focus on metallothionein. Methods: The neonatal rat cardiomyocytes hypoxia / reoxygenation model was established. The cardiomyocytes were divided into normal control group, hypoxia / reoxygenation group and aconite polysaccharide group. In hypoxia / reoxygenation group, cardiomyocytes were exposed to hypoxia for 3 hours and then reoxygenated for 6 hours. The monkshood polysaccharide group was treated with monkshood polysaccharide of 10.0,1.0,0.1 g L-1 respectively for 24 h and then hypoxia for 3 h Oxygen 6 h. The content of metallothionein was detected by ELISA, the apoptosis rate was detected by flow cytometry, the content of malondialdehyde (MDA) and the content of lactate dehydrogenase (LDH) in the cell culture medium were determined. Results: Compared with the hypoxia / reoxygenation group, the aconite polysaccharide could increase the synthesis of metallothionein in a dose-dependent manner, reduce the production of MDA and the release of LDH, and inhibit the apoptosis of cardiomyocytes, and play a role in 10.0 gL-1 Peak. CONCLUSION: Aconite polysaccharide has a protective effect on hypoxia-reoxygenation cardiomyocyte injury. Its mechanism is related to the effect of aconite polysaccharide on the synthesis of metallothionein, anti-oxidative stress and inhibition of cardiomyocyte apoptosis.