芒果苷对大鼠骨髓间充质干细胞缺氧损伤的保护作用

目的研究芒果苷对大鼠骨髓间充质干细胞(MSCs)缺氧损伤的凋亡保护机制。方法利用不同浓度的氯化钴(CoCl)建立细胞缺氧模型,检测MSCs凋亡率,获得最佳CoCl2应用浓度;利用不同浓度的芒果苷2(Mangiferin)对CoCl2建立的缺氧损伤模型进行干预,检测其对MSCs缺氧损伤模型的保护作用;通过MTT和Western blot方法分别测定各组细胞中Caspase3、Bcl-2及Bax等凋亡相关基因的蛋白表达情况。结果芒果苷对大鼠MSCs缺氧损伤具有保护作用,呈浓度依赖性;随着芒果苷浓度的增加,大鼠MSCs在缺氧损伤模型下的凋亡率逐步减少(P<0.05)。氯化钴可引起Caspase3、Bax等凋亡相关基因的蛋白表达上调,Bcl-2基因的蛋白表达下调。芒果苷能抑制氯化钴引起的Caspase3、Bax等凋亡相关基因蛋白表达的上调(<0.05)及减少Bcl-2基因蛋白表达的下调(P<0.05)。结论芒果苷对大鼠MSCs缺氧损伤诱发的凋亡具有浓度依赖性保护作用。

The protective effect of Mangiferin on bone marrow derived mesenchymal stem cells apoptosis caused by hypoxic injury in rats

Objective To observe the protective effect and possible mechanism of Mangiferin on bone marrow derived mesenchymal stem cells(BMSCs) apoptosis caused by hypoxic injury in rats.Methods The hypoxia model was established using different concentrations of CoCl2,the apoptosis rate of BMSCs was determined by MTT,the expressions of Caspase 3,Bcl-2 and Bax were detected by Western blotting.Results Mangiferin inhibited the apoptosis of BMSCs and had a protective effect on BMSCs hypoxic injury,with dose-dependent manner(<0.05).The expression levels of Caspase 3 and Bax proteins were upregulated,while the Bcl-2 level was downregulated in BMSCs injuried by hypoxia.Mangiferin inhibited the upregulation of Caspase 3 and Bax,and reduced the downregulated of Bcl-2(<0.05).Conclusion Mangiferin has a protective effect on the apoptosis of BMSCs induced byhypoxic injury.