Effect of <italic style="font-style: italic">Shenqi Jianxin Formula</italic>（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure

XIE Peichi; LIU Pan; DING Zitong; BAI Jingyi; PANG Deqi; DAI Xiaohua

doi:10.13288/j.11-2166/r.2026.04.017

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Effect of Shenqi Jianxin Formula（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure

更新时间：2026-02-10

- Effect of Shenqi Jianxin Formula（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure
- Journal of Traditional Chinese Medicine Vol. 67, Issue 4, Pages: 447-455(2026)
- 作者机构：
  
  1.安徽中医药大学第一临床医学院，安徽省合肥市梅山路117号，230000
  2.安徽中医药大学中医学院
  3.安徽中医药大学第一附属医院
- 作者简介：
- 基金信息：
- DOI：10.13288/j.11-2166/r.2026.04.017
  CLC：
- Received：27 August 2025，
  
  Revised：2025-12-15，
  
  Published：17 February 2026
- 稿件说明：
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谢沛池,刘攀,丁子彤等.参芪健心方对慢性心力衰竭模型大鼠心脏组织线粒体自噬及PINK1/Parkin信号通路的影响[J].中医杂志,2026,67(04):447-455.

XIE Peichi,LIU Pan,DING Zitong,et al.Effect of Shenqi Jianxin Formula（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure[J].Journal of Traditional Chinese Medicine,2026,67(04):447-455.
谢沛池,刘攀,丁子彤等.参芪健心方对慢性心力衰竭模型大鼠心脏组织线粒体自噬及PINK1/Parkin信号通路的影响[J].中医杂志,2026,67(04):447-455. DOI： 10.13288/j.11-2166/r.2026.04.017.

XIE Peichi,LIU Pan,DING Zitong,et al.Effect of Shenqi Jianxin Formula（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure[J].Journal of Traditional Chinese Medicine,2026,67(04):447-455. DOI： 10.13288/j.11-2166/r.2026.04.017.

摘要

目的

从PTEN诱导激酶1（PINK1）/E3泛素连接酶（Parkin）通路调控线粒体自噬角度探讨参芪健心方治疗慢性心力衰竭（CHF）的可能作用机制。

方法

SD雄性大鼠采用腹主动脉缩窄术建立大鼠CHF模型，将造模成功的24只大鼠随机分为模型组、沙库巴曲缬沙坦组及参芪健心低、高剂量组，每组6只；另取6只大鼠设为假手术组，仅分离腹主动脉后即复位关腹。参芪健心低、高剂量组大鼠分别给予参芪健心方混悬液4.41、17.64 g/（kg·d）灌胃，沙库巴曲缬沙坦组大鼠给予沙库巴曲缬沙坦钠片10 mg/（kg·d）混悬液灌胃，假手术组和模型组大鼠予10 ml/（kg·d）生理盐水灌胃，均连续干预4周。检测心功能指标左心室射血分数（LVEF）、左室短轴收缩率（LVFS），血清脑钠肽（BNP）含量，HE染色和Masson染色进行心肌组织病理观察，透射电子显微镜观察心脏组织超微结构，Rt-qPCR法检测大鼠心肌组织PINK1/Parkin通路和自噬相关蛋白［包括苄氯素1（Beclin-1）、p62、微管相关蛋白1轻链3（LC3）］及mRNA表达。

结果

与假手术组比较，模型组大鼠LVEF、LVFS水平均显著降低，血清BNP含量升高，心脏组织中

PINK1、Parkin、Beclin1

mRNA及其蛋白水平降低，

p62

mRNA及其蛋白水平升高，微管相关蛋白1轻链3β（

LC3B

） mRNA、磷酸化PTEN诱导激酶1（p-PINK1）、磷酸化E3泛素连接酶（p-Parkin）蛋白及微管相关蛋白轻链3蛋白Ⅱ与微管相关蛋白轻链3蛋白Ⅰ的比值（LC3Ⅱ/LC3Ⅰ）均显著降低（

＜0.05）；病理结果显示，模型组大鼠心肌细胞明显水肿、坏死及变性，心肌纤维排列紊乱增多，并伴有广泛炎性细胞浸润，线粒体中、重度肿胀，少数线粒体空泡变，视野内未见明显自噬。与模型组比较，参芪健心高剂量组和沙库巴曲缬沙坦组上述各指标均显著改善（

＜0.05），且参芪健心高剂量组各指标改善优于参芪健心低剂量组（

＜0.05），参芪健心高剂量组心肌肌原纤维排列规整、走向有序，横纹结构清晰，坏死细胞显著减少，偶见自噬溶酶体。

结论

参芪健心方通过激活心肌组织PINK1/Parkin信号通路，增强线粒体自噬，清除功能失调的线粒体，从而改善心功能延缓CHF的进展。

Abstract

Objective

To explore the potential mechanism of

Shenqi Jianxin Formula

（参芪健心方） in the treatment of chronic heart failure （CHF） from the perspective of regulating mitochondrial autophagy via the PTEN-induced kinase 1 （PINK1）/E3 ubiquitin ligase （Parkin） pathway.

Methods

Male SD rats were subjected to abdominal aortic constriction to establish the CHF model. Twenty-four successfully modeled rats were randomly divided into the model group， sacubitril/valsartan group， and low- and high-dose

Shenqi Jianxin Formula

groups， with 6 rats in each group. Six other rats were set as the sham surgery group， which were only separated the abdominal aorta and then closed the abdomen. Rats in the low-dose and high-dose

Shenqi Jianxin Formula

groups were given intragastric administration of

Shenqi Jianxin Formula

suspension at doses of 4.41 g/（kg·d） and 17.64 g/（kg·d）， respectively； the sacubitril/valsartan group received intragastric administration of sacubitril/valsartan sodium tablet suspension at 10 mg/（kg·d）； the sham surgery group and the model group were given normal saline at 10 ml/（kg·d） via intragastric gavage. The intervention lasted for 4 consecutive weeks. Cardiac function indices including left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were detected， and serum brain natriure

tic peptide （BNP） content was measured. HE staining and Masson staining were used to observe myocardial histopathological changes. Transmission electron microscopy was employed to examine the ultrastructure of cardiac tissues. Quantitative real-time polymerase chain reaction （Rt-qPCR） was performed to determine the mRNA expressions of PINK1/Parkin pathway-related factors and autophagy-associated proteins including Beclin-1， p62， and microtubule-associated protein 1 light chain 3 （LC3） in myocardial tissues.

Results

Compared with the sham surgery group， the model group showed significant decreases in LVEF and LVFS levels， an increase in serum BNP content， down-regulated mRNA and protein expressions of

PINK1

，

Parkin

and

Beclin

in cardiac tissues， up-regulated mRNA and protein expressions of

p62

， as well as significant reductions in

LC3B

mRNA expression， phosphorylated PTEN-induced kinase 1 （p-PINK1） and phosphorylated E3 ubiquitin ligase （p-Parkin） protein levels， and the ratio of microtubule-associated protein 1 light chain 3-Ⅱ to microtubule-associated protein 1 light chain 3-Ⅰ （LC3Ⅱ/LC3Ⅰ）（

＜0.05）. Pathological results revealed obvious myocardial cell edema， necrosis and degeneration， increased disorder of myocardial fiber arrangement， extensive inflammatory cell infiltration， moderate to severe mitochondrial swelling， a few mitochondrial vacuolar changes， and no obvious autophagy in the field of vision in the model group. Compared with the model group， all the above indicators were significantly improved in the high-dose

Shenqi Jianxin Formula

group and the sacubitril/valsartan group （

＜0.05）. Moreover， the improvement of each index in the high-dose

Shenqi Jianxin Formula

group was superior to that in the low-dose group （

＜0.05）. In the high-dose

Shenqi Jianxin Formula

group， my

ocardial myofibrils were arranged regularly with orderly orientation， the striated structure was clear， and necrotic cells significantly reduced.

Conclusion

Shenqi Jianxin Formula

can activate the PINK1/Parkin signaling pathway in myocardial tissues， enhance mitochondrial autophagy， and clear dysfunctional mitochondria， thereby improving cardiac function and delaying the progression of CHF.

关键词

Keywords

references

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School of Chinese Medicine， Anhui University of Chinese Medicine

Anhui Hospital of Integrated Chinese and Western Medicine

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⁰

Effect of Shenqi Jianxin Formula（参芪健心方）on Mitochondrial Autophagy and the PINK1/Parkin Signaling Pathway in Cardiac Tissues in Chronic Heart Failure

DOI：10.13288/j.11-2166/r.2026.04.017

摘要

Abstract

关键词

Keywords

references