Open Access

Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy

  • Authors:
    • Ran Xia
    • Wei Wang
    • Bing Gao
    • Qiang Ma
    • Jing Wang
    • Xiaohua Dai
    • Qingling Li
  • View Affiliations

  • Published online on: March 30, 2022     https://doi.org/10.3892/etm.2022.11286
  • Article Number: 359
  • Copyright: © Xia et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Moxibustion (MOX) is a traditional Chinese medicine preparation, which has been clinically used to treat cardiac diseases in recent years. The present study aimed to examine the protective effects and possible mechanisms of MOX on doxorubicin (DOX)‑induced chronic heart failure (CHF) in rats. The animals were divided into five groups, including the Control (normal saline), DOX (doxorubicin 15 mg/kg), MOX (doxorubicin 15 mg/kg + moxibustion), BEN (doxorubicin 15 mg/kg + benazepril 0.86 mg/kg) and MOX + BEN (doxorubicin 15 mg/kg + moxibustion + benazepril 0.86 mg/kg) groups. After three weeks, echocardiography was performed to assess cardiac function and structure, including left ventricular internal diameter in systole, ejection fraction and fractional shortening (FS). Serum brain natriuretic peptide levels and adenosine triphosphate (ATP) levels were measured by enzyme‑linked immunosorbent assay and ATP assay. Cardiac pathology was assessed by hematoxylin and eosin and Masson's trichrome staining. Cardiac ultrastructure and the number of autophagosomes formed were visualized by transmission electron microscopy. Western blotting was performed to assess mitochondrial dynamics, autophagy proteins and mitochondrial autophagy‑related pathway proteins. The expression levels of these genes were assessed by reverse transcription‑quantitative PCR. The results indicated MOX could improve cardiac function, increased cardiac ATP levels and reduced myocardial fibrosis. Western blotting indicated that MOX treatment elevated the expression of optic atrophy 1 protein (OPA1), while decreasing the expression of dynamin‑related protein 1 and mitochondrial fission 1 protein. In addition, MOX inhibited autophagy, as evidenced by decreased number of autophagosomes, reduced LC3II/LC3I ratio and increased p62 expression. Furthermore, MOX downregulated DOX‑induced FUNDC1 signaling pathway. In summary, MOX has protective effects on DOX‑induced CHF in rats, promoting mitochondrial fusion while inhibiting mitochondrial fission and mitophagy. The underlying mechanisms may be related to the inhibition of the FUNDC1 signaling pathway.
View Figures
View References

Related Articles

Journal Cover

May-2022
Volume 23 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Xia R, Wang W, Gao B, Ma Q, Wang J, Dai X and Li Q: Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy. Exp Ther Med 23: 359, 2022
APA
Xia, R., Wang, W., Gao, B., Ma, Q., Wang, J., Dai, X., & Li, Q. (2022). Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy. Experimental and Therapeutic Medicine, 23, 359. https://doi.org/10.3892/etm.2022.11286
MLA
Xia, R., Wang, W., Gao, B., Ma, Q., Wang, J., Dai, X., Li, Q."Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy". Experimental and Therapeutic Medicine 23.5 (2022): 359.
Chicago
Xia, R., Wang, W., Gao, B., Ma, Q., Wang, J., Dai, X., Li, Q."Moxibustion alleviates chronic heart failure by regulating mitochondrial dynamics and inhibiting autophagy". Experimental and Therapeutic Medicine 23, no. 5 (2022): 359. https://doi.org/10.3892/etm.2022.11286