摘要
目的基于miR-503-5p/Bcl-2通路介导的细胞凋亡机制,探究清热化瘀方对脑缺血再灌注(ischemia/reperfusion,I/R)大鼠脑组织损伤的保护效应并探讨其作用机制。方法SD大鼠分为正常组、假手术组、模型组、清热化瘀方组。线栓法建立脑I/R大鼠模型,采用清热化瘀方剂灌胃治疗。采用RT-qPCR、Western blot法分别检测缺血脑组织中miR-503-5p及Bcl-2、Bax、caspase-3、caspase-8、caspase-9 mRNA和蛋白表达。TUNEL染色检测大鼠脑组织细胞凋亡情况。结果大鼠I/R可降低脑组织中Bcl-2表达,升高miR-503-5p、Bax、caspase-3、caspase-8、caspase-9表达及脑组织凋亡率。清热化瘀方治疗后可升高脑组织中Bcl-2表达,降低miR-503-5p、Bax、caspase-3、caspase-8、caspase-9表达及脑组织凋亡率。结论清热化瘀方可抑制脑I/R大鼠脑组织细胞凋亡,其机制可能与抑制miR-503-5p、Bax及caspase家族表达、上调Bcl-2表达有关。
Objective Based on the mechanism of apoptosis mediated by miR-503-5p/Bcl-2 pathway,to explore the protective effect and mechanism of Qingre Huayu prescription on brain tissue damage in rats with cerebral ischemia/reperfusion(I/R).Methods SD rats were divided into normal group,sham operation group,model group,and Qingre Huayu prescription group.The rat model of cerebral I/R was established by thread suppository method,and treated by Qingre Huayu prescription.The expressions of miR-503-5p and the mRNA and protein expressions of Bcl-2,Bax,caspase-3,caspase-8 and caspase-9 were detected by RT qPCR and Western blot.Apoptosis was detected by TUNEL staining.Results After I/R,the expression of Bcl-2 was decreased,the expression of miR-503-5p,Bax,caspase-3,caspase-8,caspase-9 and the apoptosis rate of brain tissue were increased.After treatment with Qingre Huayu prescription,the expression of Bcl-2 in the brain tissue of the group was increased,and the expression of miR-503-5p,Bax,caspase-3,caspase-8,caspase-9 and the apoptosis rate of brain tissue were reduced.Conclusion Qingre Huayu prescription could inhibit brain tissue cell apoptosis in rats with cerebral I/R,and its mechanism may be related to inhibiting the expression of miR-503-5p,Bax and caspase families and up-regulating the expression of Bcl-2.
作者
秦红玲
胡跃强
农必华
陈炜
程越
卢健锋
谭璐璐
Qin Hongling;Hu Yueqiang;Nong Bihua(The First Affiliated Hospital of Guangxi University of Chinese Medicine,Guangxi 530023,China)
出处
《医学研究杂志》
2021年第9期45-49,共5页
Journal of Medical Research
基金
国家自然科学基金青年科学基金资助项目(81704034)
广西科技计划项目(桂科AD20238028)。
