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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。
Objective To study the protective mechanism of mangiferin on apoptosis of rat bone marrow mesenchymal stem cells (MSCs) under hypoxia. Methods The model of cell hypoxia was established by using different concentrations of cobalt chloride (CoCl) to detect the apoptosis rate of MSCs, and the optimal concentration of CoCl2 was obtained. The model of hypoxia injury induced by CoCl2 was intervened by using different concentrations of Mangiferin (2) , And detected their protective effects on hypoxia injury of MSCs. The protein expressions of apoptosis-related genes such as Caspase3, Bcl-2 and Bax in each group were determined by MTT and Western blot respectively. Results Mangiferin had a protective effect on hypoxia injury of MSCs in a concentration-dependent manner. With the increase of mangiferin concentration, the apoptosis rate of MSCs gradually decreased in the hypoxic injury model (P <0.05). Cobalt chloride could induce the up-regulation of the apoptosis-related genes such as Caspase3, Bax and down-regulate the protein expression of Bcl-2. Mangiferin inhibited the up-regulation (P <0.05) of the apoptosis-related genes such as Caspase3 and Bax induced by cobalt chloride (P <0.05) and decreased the expression of Bcl-2 protein. Conclusion Mangiferin has a concentration-dependent protective effect on apoptosis induced by hypoxia in rat MSCs.