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.