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目的探讨丹参酮ⅡA在体外对海马神经元细胞放射性损伤的影响,以及其在放射性损伤保护过程中的相关机制。方法体外培养海马神经元细胞株HT-22,实验分为对照组(Control)、照射组(RT)、照射+丹参酮ⅡA处理组(RT+Tan)、照射+丹参酮ⅡA+自噬抑制剂3-Methyladenine(3-MA)处理组(RT+Tan+3-MA)。采用MTT法检测各组细胞的存活分数,流式细胞技术检测细胞凋亡,Western blot检测自噬相关蛋白LC3-I、LC3-Ⅱ的表达水平。结果照射后海马神经元细胞存活分数下降,而丹参酮ⅡA能提高放射线照射后海马神经元细胞的存活分数,并减少细胞凋亡。相对于单纯照射组,RT+Tan组的海马神经元细胞HT-22的自噬相关蛋白LC3-Ⅱ的表达上升。而加入自噬抑制剂3-MA后,放射处理后的海马神经元细胞LC3蛋白表达下降,且存活分数明显下降。结论丹参酮ⅡA能明显减轻放射线在体外对海马神经元细胞的放射损伤作用,其保护机制可能与调节放疗过程中自噬相关。
Objective To investigate the effect of tanshinone ⅡA on radioactive injury of hippocampal neurons in vitro and the related mechanisms during the protection of radiation injury. Methods The hippocampal neuronal cell line HT-22 was cultured in vitro. The experiment was divided into control group, irradiation group, irradiation + tanshinoneⅡA treatment group (RT + Tan), irradiation + tanshinoneⅡA + autophagy inhibitor 3-Methyladenine (3-MA) treatment group (RT + Tan + 3-MA). Cell viability was measured by MTT assay. Apoptosis was detected by flow cytometry. Western blot was used to detect the expression of LC3-I and LC3-II. Results The survival of hippocampal neurons decreased after irradiation, while tanshinone ⅡA increased the survival of hippocampal neurons after irradiation and decreased the apoptosis. Compared with the irradiation alone group, the expression of autophagy-related protein LC3-Ⅱ of HT-22 in hippocampal neurons of RT + Tan group increased. After addition of autophagy inhibitor 3-MA, the expression of LC3 protein in hippocampal neurons decreased, and the survival score decreased significantly. Conclusion Tanshinone ⅡA can obviously reduce the radiation injury of hippocampal neurons in vitro by radiation, and its protective mechanism may be related to the regulation of autophagy during radiotherapy.