Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2026
Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Bing Gao, Pan Liu, Lan L I, Tiantian Gong, Ling Zhu, Lingji L I, Ran Xia, Qiang M A, Jing H U, Jing Wang
Аннотация
OBJECTIVE: To explore the mechanism by which moxibustion alleviates autophagy and inhibits ferroptosis, thereby improving myocardial fibrosis in rats with post-myocardial infarction heart failure (post-MI HF).
METHODS: We used a rat model of post-MI HF rats. Interventions included moxibustion and intraperitoneal injection of rapamycin (RAPA) along with assessing echocardiography, cardiac pathology, myocardial mitochondrial morphology, co-immunofluorescence, transmission electron microscope, Western blotting, and reverse transcriptase-quantitative polymerase chain reaction.
RESULTS: Moxibustion improves the left ventricular ejection fraction and fractional shortening, myocardial cell morphology, and myocardial fibrosis levels induced by post-MI HF. In addition, it reduces the immunofluorescence co-localization intensity of nuclear receptor coactivator 4 (NCOA4) and microtubule-associated protein 1A/1B light chain 3 and decreases the level of intracellular free iron. It suppresses autophagy and ferroptosis-related indicators, downregulates NCOA4 expression, upregulates glutathione peroxidase 4 expression, and decreases lipid peroxidation levels. The activation of autophagy increases NCOA4 expression and promotes ferroptosis. Furthermore, moxibustion counteracts the effects of RAPA.
CONCLUSIONS: Moxibustion can alleviate myocardial fibrosis and exert cardioprotective effects by regulating autophagy and inhibiting ferroptosis. Our findings indicate that targeting autophagy-induced ferroptosis may serve as a novel therapeutic approach for the treatment of post-MI HF.
METHODS: We used a rat model of post-MI HF rats. Interventions included moxibustion and intraperitoneal injection of rapamycin (RAPA) along with assessing echocardiography, cardiac pathology, myocardial mitochondrial morphology, co-immunofluorescence, transmission electron microscope, Western blotting, and reverse transcriptase-quantitative polymerase chain reaction.
RESULTS: Moxibustion improves the left ventricular ejection fraction and fractional shortening, myocardial cell morphology, and myocardial fibrosis levels induced by post-MI HF. In addition, it reduces the immunofluorescence co-localization intensity of nuclear receptor coactivator 4 (NCOA4) and microtubule-associated protein 1A/1B light chain 3 and decreases the level of intracellular free iron. It suppresses autophagy and ferroptosis-related indicators, downregulates NCOA4 expression, upregulates glutathione peroxidase 4 expression, and decreases lipid peroxidation levels. The activation of autophagy increases NCOA4 expression and promotes ferroptosis. Furthermore, moxibustion counteracts the effects of RAPA.
CONCLUSIONS: Moxibustion can alleviate myocardial fibrosis and exert cardioprotective effects by regulating autophagy and inhibiting ferroptosis. Our findings indicate that targeting autophagy-induced ferroptosis may serve as a novel therapeutic approach for the treatment of post-MI HF.