Mechanism of Yixin Futing Yin (益心附葶饮) in Treating Heart Failure by Regulating Cardiac Mitophagy through the BNIP3/NIX Pathway
Author：ZHANG Xueli1, LEI Yuanlin2, YAO Jia2, XIONG Ziyan2
Unit：1.Fifth Clinical Medical College of Shaanxi University of Chinese Medicine, Xi'an Shaanxi 710000, China; 2.Xi'an Hospital of Traditional Chinese Medicine, Xi'an Shaanxi 710000, China
Quote：引用：张雪莉，雷瑗琳，姚佳，熊紫嫣.益心附葶饮通过BNIP3/NIX通路调控心肌线粒体自噬治疗心力衰竭的机制[J].中医药导报,2026,32(4):48-54.
DOI：10.13862/j.cn43-1446/r.2026.04.009
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Abstract：
Objective: To investigate the mechanism of Yixin Futing Yin in treating heart failure by regulating mitophagy in mouse cardiomyocytes (HL-1) through the BNIP3/NIX signaling pathway. Methods: Totally 30 SD rat were randomly divided into normal group, Yixin Futing Yin low-dose group (26.25 mg/kg), Yixin Futing Yin medium-dose group (52.50 mg/kg), Yixin Futing Yin high-dose group (105.00 mg/kg) and trimetazidine group (10 mg/kg), 6 mice in each group. The drug was administered by gavage for 14 consecutive days, and blood was collected from the abdominal aorta for the preparation of drug-containing serum of Yixin Futing Yin. The HL-1 cells were subdivided into normal group, model group, Yixin Futing Yin low-dose group, Yixin Futing Yin medium-dose group, Yixin Futing Yin high-dose group and trimetazidine group, and the cells were cultured by adding the drug-containing serum. The activity of the cells in each group was detected by CCK-8. The ROS level of the cells in each group was detected by flow cytometry, and Western blottingand was used to detect the protein expressions level of Beclin-1, Atg7, p-P62/P62, LC3, BNIP3 and NIX. Results: Compared with the normal group, the model group showed decreased cell viability (P<0.01), increased ROS levels (P<0.01), and elevated protein expression of Beclin-1, Atg7, p-P62/P62, LC3, BNIP3, and NIX (P<0.01), indicating that the cells were under oxidative stress and initiated an adaptive response mainly characterized by autophagy activation. Compared with the model group, the Yixin Futing Yin low-dose group, Yixin Futing Yin medium-dose group, Yixin Futing Yin high-dose group and trimetazidine group showed increased cell viability (P<0.05), decreased ROS levels (P<0.01), and reduced protein expression of Beclin-1, Atg7, p-P62/P62, LC3, BNIP3, and NIX (P＜0.05 or P<0.01). The therapeutic effect of Yixin Futing Yin exhibited a dose-dependent relationship, and the high-dose Yixin Futing Yin was non-inferior to trimetazidine. Conclusion: Yixin Futing Yin may treat heart failure by regulating cellular mitophagy through inhibition of BNIP3/NIX protein expression.
Key words：heart failure; Yixin Futing Yin; mitophagy; BNIP3/NIX pathway; cardiomyocytes; rat
摘要：
目的：探讨益心附葶饮通过BNIP3/NIX信号通路调控小鼠心肌（HL-1）细胞线粒体自噬治疗心力衰竭的作用机制。方法：将30只SD大鼠随机分为正常组、益心附葶饮低剂量组（26.25 mg/kg）、益心附葶饮中剂量组（52.50 mg/kg）、益心附葶饮高剂量组（105.00 mg/kg）、曲美他嗪组（10 mg/kg），每组各6只。连续14 d灌胃给药，给药结束后，采集腹主动脉血，制备益心附葶饮含药血清。将HL-1细胞分为正常组，模型组，益心附葶饮低、中、高剂量组，曲美他嗪组，分别加入相应含药血清培养细胞。细胞计数试剂盒-8（CCK-8）法检测细胞活性；流式细胞术检测细胞活性氧（ROS）水平；蛋白质印迹（Western blotting）法检测细胞Beclin-1、Atg7、p-P62/P62、LC3、BNIP3、NIX蛋白表达水平。结果：与正常组比较，模型组细胞活性降低（P＜0.01），ROS水平升高（P＜0.01），Beclin-1、Atg7、p-P62/P62、LC3、BNIP3、NIX蛋白表达升高（P＜0.01），提示细胞处于氧化应激状态，并启动了以自噬激活为主的适应性反应；与模型组比较，益心附葶饮低、中、高剂量组及曲美他嗪组细胞活性升高（P＜0.05），ROS水平下降（P＜0.01），Beclin-1、Atg7、p-P62/P62、LC3、BNIP3、NIX蛋白表达下降（P＜0.05或P＜0.01），益心附葶饮疗效呈现剂量-效应依赖关系，且高剂量益心附葶饮疗效不劣于曲美他嗪。结论：益心附葶饮可能通过抑制BNIP3/NIX蛋白表达，从而调控细胞线粒体自噬，进而治疗心力衰竭。
关键词：心力衰竭；益心附葶饮；线粒体自噬；BNIP3/NIX通路；心肌细胞；大鼠
Release time：2026-04-26
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