PulseExploreJournal ClubDebatesTrendingResearchersJournals
Instagram
HomeExploreJournal ClubTrending
Synapse
⌘+K
Synapse
February 2, 2021Evidence-based Complementary and Alternative Medicine13 citationsOpen Access

Moxibustion Improves Chronic Heart Failure by Inhibiting Autophagy and Inflammation via Upregulation of mTOR Expression

QLQingling LiWWWei WangQMQiang Ma

Key Result

Moxibustion significantly improved heart function and structure in rats with chronic heart failure, possibly by inhibiting excessive autophagy and reducing inflammation via mTOR upregulation.

Key Points

  • This research investigates whether moxibustion reduces inflammation and autophagy via mTOR regulation in chronic heart failure.
  • Evaluated cardiac function using echocardiography in rats with heart failure.
  • Measured BNP levels through enzyme-linked immunosorbent assay (ELISA).
  • Analyzed mTOR expression via western blotting and PCR for autophagy-associated genes.
  • Moxibustion significantly improved cardiac function and structure in rats with heart failure.
  • Moxibustion elevated mTOR expression, inhibiting autophagy-related genes and reducing inflammation markers.
  • Rapamycin partially mitigated the positive effects of moxibustion on cardiac function.

Structured PICO

Does moxibustion improve cardiac function and reduce inflammation in rats with heart failure?

P
Population
Rats with chronic heart failure.
I
Intervention
moxibustion
O
Outcome
cardiac function and structure (HR, LA, LV, LVPW, IVS, EF, FS), BNP and NT-pro BNP levels, mTOR expression, autophagy-associated protein genes, and inflammatory responsesurrogate

Moxibustion protects cardiac function in rats with heart failure by inhibiting excessive autophagy and reducing inflammation through mTOR upregulation.

Abstract

How moxibustion improves chronic heart failure is extremely complex and still unclear. This study aimed to explore whether moxibustion inhibits autophagy and reduces inflammation by regulating mTOR expression to induce myocardial protective effects and alleviate symptoms associated with chronic heart failure. Echocardiography was used to detect cardiac function and cardiac structure of rats, including heart rate (HR), left atrium diameter (LA), left ventricular diameter (LV), left ventricular posterior wall (LVPW), interventricular septum (IVS), ejection fraction (EF), and fractional shortening (FS). BNP and NT-pro BNP levels were measured by enzyme-linked immunosorbent assay (ELISA). Autophagy-associated protein (ATG) genes and mTOR were detected by PCR. The expression of mTOR and phosphorylated-mTOR was detected through western blotting of proteins from myocardial tissue samples. The left ventricular inflammatory response was detected by immunohistochemistry and included ICAM-1, VCAM-1, MMP-2, and MMP-9 expression. The relationship between autophagy and inflammation was analyzed by correlation analysis. The results from echocardiography and ELISA showed that moxibustion could significantly improve heart function and structure. Western blot and PCR results showed that moxibustion treatment elevated mTOR expression. Further, moxibustion could inhibit autophagy and regulate the expression of key autophagy-related genes, including Vps34, ATG3, ATG5, ATG7, ATG12, and ATG13. By contrast, rapamycin could partially reduce the effects of moxibustion. Immunohistochemistry results indicated that moxibustion could reduce myocardial inflammation. Moreover, there was a positive correlation between autophagy and inflammation. Moxibustion can protect cardiac function in rats with heart failure, possibly inhibiting excessive autophagy of cardiomyocytes and reducing inflammatory reactions through the elevation of mTOR expression.

Ask AI
Helpful
Bookmark
Share
View Full Paper

Cite This Study

Li et al. (2021) studied Chronic heart failure. Moxibustion was evaluated on Cardiac function and structure. Moxibustion significantly improved heart function and structure in rats with chronic heart failure, possibly by inhibiting excessive autophagy and reducing inflammation via mTOR upregulation.

synapsesocial.com/papers/6a7063be78a11c550e0a4791https://doi.org/10.1155/2021/6635876
Ask AI
Helpful
Bookmark
Share
View Full Paper