痰瘀同治方对心肌缺血再灌注损伤大鼠核因子-κB通路及心肌自噬、凋亡的影响  

Effects of Tanyu Tongzhi Formula on NF-κB Pathway, Autophagy and Antiapoptosis of Rats with Myocardial Ischemia-Reperfusion Injury

作　　者：唐丹丽[1] 崔海峰[1] 隋宇[1] 佟琳[2] 刘寨华[3] 张华敏[2] 

机构地区：[1]中国中医科学院医学实验中心,北京100700 [2]中国中医科学院中医药信息研究所,北京100700 [3]中国中医科学院中医基础理论研究所,北京100700

出　　处：《中国中医药信息杂志》2015年第12期38-42,共5页Chinese Journal of Information on Traditional Chinese Medicine

基　　金：国家自然科学基金(81202630;81373792);中国中医科学院基本科研业务费自主选题项目(ZZ2014002)

摘　　要：目的观察痰瘀同治方对心肌缺血再灌注损伤(MI/RI)大鼠核因子(NF)-κB通路及心肌自噬、凋亡的影响,探讨该方抗MI/RI作用机制。方法 40只SD大鼠随机分为假手术组、模型组、吡咯烷二硫代甲酸铵(PDTC)干预组及痰瘀同治组。可逆性冠脉左前降支结扎缺血30 min、再灌注2 h复制MI/RI模型。造模前,痰瘀同治组每日予痰瘀同治方水煎液灌胃,其他各组给予生理盐水灌胃,连续3周。RT-PCR检测各组大鼠心肌NF-κB、自噬基因Beclin-1表达,Western blot检测心肌促凋亡蛋白Bax和抗凋亡蛋白Bcl-2表达。结果与假手术组比较,模型组大鼠心肌NF-κB、Beclin-1 m RNA及Bax蛋白表达均显著增强,且Bcl-2蛋白降低(均P<0.01);与模型组比较,痰瘀同治组能抑制再灌注后NF-κB、Beclin-1 m RNA及Bax蛋白高表达(均P<0.01),且作用与PDTC干预组相当(P>0.05),痰瘀同治组能显著上调心肌Bcl-2表达,且作用优于PDTC干预组(P<0.01)。结论痰瘀同治方通过抑制NF-κB活化,改善心肌细胞凋亡,抑制自噬而达到保护心肌的作用。Objective To observe the effects of Tanyu Tongzhi Formula(TYTZF) on NF-κB pathway, autophagy and antiapoptosis of rats with myocardial ischemia-reperfusion injury(MI/RI);To investigate the mechanism of anti-MI/RI of TYTZF. Methods Forty SD rats were randomly divided into sham-operation group, model group, PDTC and TYTZF groups. The model of ischemia reperfusion of the myocardium was reproduced by ligation of left descending artery for 30 min and followed by releasing the ligation for 2 hours in rats. The TYTZF group was fed with TYTZF decoction for gavage, while the other groups were fed with normal saline for 3 weeks. The gene expression levels of NF-κB and Beclin-1 were determined with RT-PCR;the protein expressions of Bax and Bcl-2 were detected by Western blot. Results Compared with the sham-operation group, both the expressions of NF-κB and Beclin-1 m RNA and the protein expression of Bax significantly increased, while the protein expression of Bcl-2 decreased in the model group(P <0.01). Compared with the model group, the TYTZF group down-regulated the expressions of NF-κB, Beclin-1 m RNA and Bax, and up-regulated protein expression of Bcl-2(P <0.01). TYTZF showed better effects on up-regulating the level of Bcl-2 than PDTC(P <0.01). Conclusion TYTZF could play a role in the protection of the myocardium by inhibiting the activation of NF-κB, and preventing the occurrence of apoptosis and autophagy of myocardial cell.

关 键 词：心肌缺血再灌注损伤 核因子-ΚB 自噬 凋亡 痰瘀同治方 大鼠 

分 类 号：R285.5[医药卫生—中药学]