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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 effects of tanshinone IIA on the radiation injury of hippocampal neurons in vitro and explore its mechanism in the course of radiation injury.Methods The hippocampal neuron cell line HT?22 was cultured in vitro. The experiment included four groups:control group(Control),irradiation group(RT),irradiation +Tanshinone IIA treatment group(RT+Tan),and irradiation+Tanshinone IIA+autophagy inhibitor 3?Methyladenine(3?MA)treatment group(RT+Tan+3?MA). The cell survival fraction was detected by MTT assay. Apoptosis was detected by flow cytometry. The expression levels of autophagy?related proteins LC3?I and LC3?II were detected by Western blot. Results The survival fraction of hippocampal neurons decreased after irradiation , while tanshinone IIA increased the survival fraction of hippocampal neurons and decreased the apoptosis rate after irradiation. The expression of autophagy?related protein LC 3?II in hippocampal neuron HT?22 cells treated with tanshinone IIA and irradiation treatment increased significantly compared with that of irradiated group. The expression of LC3 protein in hippocampal neurons decreased again after 3?MA treatment, and the survival fraction decreased significantly after treatment with autophagy inhibitor 3?MA. Conclusion Tanshinone IIA can significantly attenuate the radiation injury of hippocampal neurons in vitro,and its protective mechanism may be related to autophagy during the course of radiotherapy.