Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (2): 339-349.DOI: 10.19852/j.cnki.jtcm.2026.02.007
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Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure
GAO Bing1, LIU Pan1, LI Lan2, GONG Tiantian2, ZHU Ling2, LI Lingji1, XIA Ran1,3, MA Qiang2,3, HU Jing1, WANG Jing1,3,4(
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College of Traditional Chinese Medicine ,Anhui University of Chinese Medicine Hefei 230012, China
2Acupuncture and moxibustion and Massage College ,Anhui University of Chinese Medicine Hefei 230012, China
3Key Laboratory of Xin’an Medical Ministry of Education ,Anhui University of Chinese Medicine Hefei 230012, China
4Center for Xin’an Medicine and Modernization of Traditional Chinese Medicine of IHM Hefei 230012, China
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Received:2024-11-03Accepted:2025-05-15Online:2026-04-15Published:2026-04-04 -
Contact:Dr. WANG Jing, College of Traditional Chinese Medicine, Anhui University of Chinese Medicine, Hefei 230012, China. Wangjing2161@126.com; Telephone: +86-13865912237 -
Supported by:National Natural Science Foundation of China: Research on the Cardiomyoprotective Effect Mechanism of Moxibustion Regulating the Mammalian Target of Rapamycin Signaling Pathway to Inhibit Autophagy(81574084);Natural Science Research Project of Colleges and Universities in Anhui Province, China: Exploring the Mechanism of Moxibustion Anti-chronic Heart Failure Fibrosis Based on MicroRNA-21/Phosphatase and Tensin Homolog/mTOR Signaling Pathway-mediated Circular RNA PAN3 Regulation of Cardiomyocyte Autophagy, and Investigating the Mechanism of Moxibustion in Preventing and Treating Chronic Heart Failure Myocardial Fibrosis Based on Transient Receptor Potential Vanilloid 1-regulated Calcitonin Gene-Related Peptide-mediated Vascular Endothelial Growth Factor Endothelial Nitric Oxide Synthase Signaling Pathway(kj2021a0570);Natural Science Research Project of Colleges and Universities in Anhui Province, China: Exploring the Mechanism of Moxibustion Anti-chronic Heart Failure Fibrosis Based on MicroRNA-21/Phosphatase and Tensin Homolog/mTOR Signaling Pathway-mediated Circular RNA PAN3 Regulation of Cardiomyocyte Autophagy, and Investigating the Mechanism of Moxibustion in Preventing and Treating Chronic Heart Failure Myocardial Fibrosis Based on Transient Receptor Potential Vanilloid 1-regulated Calcitonin Gene-Related Peptide-mediated Vascular Endothelial Growth Factor Endothelial Nitric Oxide Synthase Signaling Pathway(2023AH050796);Special Project of Xin'an Medical and Traditional Chinese Medicine Modernization Research Institute of Great Health Research Institute: Research on the Academic Thoughts of Xin'an Medical Expert Wu Yiding in Treating Fever with Moxibustion and the Application of Moxibustion in the Treatment of Epidemic Viral Pneumonia(2023CXMMTCM022)
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GAO Bing, LIU Pan, LI Lan, GONG Tiantian, ZHU Ling, LI Lingji, XIA Ran, MA Qiang, HU Jing, WANG Jing. Moxibustion alleviates autophagy and inhibits ferroptosis to improve cardiac function in rats with post-myocardial infarction heart failure[J]. Journal of Traditional Chinese Medicine, 2026, 46(2): 339-349.
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Figure 1 Protective effect of moxibustion on myocardial injury in rats with post-MI HF A: identification model of echocardiography; A1: CON group; A2: MOD group; B: EF values; C: FS values; D: three groups of rat echocardiography; D1: CON group; D2: MOD group; D3: MOX group; E: EF values; F: FS values; G: LVIDd vales; H: LVIDs values; I: comparison of ck-MB content in 3 groups of rats; J: histochemical sections of the left ventricle were stained with HE (scale bar, 50 μm); J1: CON group; J2: MOD group; J3: MOX group. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; EF: left ventricular ejection fraction; FS: fractional shortening; LVIDd: left ventricular internal dimension in diastole; LVIDs: left ventricular internal dimension systole; ck-MB: the creatine kinase-myocardial band; HE: hematoxylin and eosin staining. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01, cP < 0.05.
Figure 1 Protective effect of moxibustion on myocardial injury in rats with post-MI HF A: identification model of echocardiography; A1: CON group; A2: MOD group; B: EF values; C: FS values; D: three groups of rat echocardiography; D1: CON group; D2: MOD group; D3: MOX group; E: EF values; F: FS values; G: LVIDd vales; H: LVIDs values; I: comparison of ck-MB content in 3 groups of rats; J: histochemical sections of the left ventricle were stained with HE (scale bar, 50 μm); J1: CON group; J2: MOD group; J3: MOX group. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; EF: left ventricular ejection fraction; FS: fractional shortening; LVIDd: left ventricular internal dimension in diastole; LVIDs: left ventricular internal dimension systole; ck-MB: the creatine kinase-myocardial band; HE: hematoxylin and eosin staining. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01, cP < 0.05.
Figure 2 Moxibustion reduces autophagy and ferritinophagy caused by post-MI HF A: immunofluorescence co-localization intensity of LC3B and NCOA4 in myocardial tissues (scale bar, 50 μm); A1: DAPI staining in CON group; A2: LC3B fluorescence staining in CON group; A3: NCOA4 fluorescence staining in CON group; A4: LC3B-NCOA4 co localization in CON group; A5: DAPI staining in MOD group; A6: LC3B fluorescence staining in MOD group; A7: NCOA4 fluorescence staining in MOD group; A8: LC3B-NCOA4 co localization in MOD group; A9: DAPI staining in MOX group; A10: LC3B fluorescence staining in MOX group; A11: NCOA4 fluorescence staining in MOX group; A12: LC3B-NCOA4 co localization in MOX group; B: content of Fe2+ in myocardial tissue; C: representative Western blot bands showing protein expression of ATG5, LC3Ⅱ/I, and β-actin in the myocardium of rats; D: quantitative analysis of ATG5 protein expression normalized to β-actin; E: quantitative analysis of LC3II/I protein expression normalized to β-actin; F: ATG5 mRNA expression levels across experimental groups; G: LC3B mRNA expression levels across experimental groups. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; LC3B: microtubule-associated proteins 1A/1B light chain 3; NCOA4: nuclear receptor coactivator 4; DAPI: 4′, 6-diamidino-2-phenylindole; Fe2+: ferrous iron; ATG5: autophagy-related protein 5; LC3II/I: microtubule-associated protein 1A/1B light chain 3. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
Figure 2 Moxibustion reduces autophagy and ferritinophagy caused by post-MI HF A: immunofluorescence co-localization intensity of LC3B and NCOA4 in myocardial tissues (scale bar, 50 μm); A1: DAPI staining in CON group; A2: LC3B fluorescence staining in CON group; A3: NCOA4 fluorescence staining in CON group; A4: LC3B-NCOA4 co localization in CON group; A5: DAPI staining in MOD group; A6: LC3B fluorescence staining in MOD group; A7: NCOA4 fluorescence staining in MOD group; A8: LC3B-NCOA4 co localization in MOD group; A9: DAPI staining in MOX group; A10: LC3B fluorescence staining in MOX group; A11: NCOA4 fluorescence staining in MOX group; A12: LC3B-NCOA4 co localization in MOX group; B: content of Fe2+ in myocardial tissue; C: representative Western blot bands showing protein expression of ATG5, LC3Ⅱ/I, and β-actin in the myocardium of rats; D: quantitative analysis of ATG5 protein expression normalized to β-actin; E: quantitative analysis of LC3II/I protein expression normalized to β-actin; F: ATG5 mRNA expression levels across experimental groups; G: LC3B mRNA expression levels across experimental groups. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; LC3B: microtubule-associated proteins 1A/1B light chain 3; NCOA4: nuclear receptor coactivator 4; DAPI: 4′, 6-diamidino-2-phenylindole; Fe2+: ferrous iron; ATG5: autophagy-related protein 5; LC3II/I: microtubule-associated protein 1A/1B light chain 3. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
Figure 3 Moxibustion inhibits post-MI HF myocardial injury-induced ferroptosis in cardiac tissue A: transmission electron microscopy observation of myocardial cells; A1: CON group; A2: MOD group; A3: MOX group; A4: RAPA group; A5: MOX + RAPA group; B: representative Western blot bands showing protein expression of NCOA4, GPX4, FTH1, and β-actin in the myocardium of rats; C: quantitative analysis of NCOA4 protein expression normalized to β-actin; D: quantitative analysis of GPX4 protein expression normalized to β-actin; E: quantitative analysis of FTH1 protein expression normalized to β-actin; F: myocardial GSH content assayed by commercial kit; G: myocardial MDA activity assayed by commercial kit; H: myocardial SOD activity assayed by commercial kit. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; GPX4: glutathione peroxidase 4; NCOA4: nuclear receptor coactivator 4; FTH1: ferritin, heavy polypeptide 1; GSH: glutathione; MDA: malondialdehyde; SOD: superoxide dismutase. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
Figure 3 Moxibustion inhibits post-MI HF myocardial injury-induced ferroptosis in cardiac tissue A: transmission electron microscopy observation of myocardial cells; A1: CON group; A2: MOD group; A3: MOX group; A4: RAPA group; A5: MOX + RAPA group; B: representative Western blot bands showing protein expression of NCOA4, GPX4, FTH1, and β-actin in the myocardium of rats; C: quantitative analysis of NCOA4 protein expression normalized to β-actin; D: quantitative analysis of GPX4 protein expression normalized to β-actin; E: quantitative analysis of FTH1 protein expression normalized to β-actin; F: myocardial GSH content assayed by commercial kit; G: myocardial MDA activity assayed by commercial kit; H: myocardial SOD activity assayed by commercial kit. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks. MI: myocardial infarction; HF: heart failure; GPX4: glutathione peroxidase 4; NCOA4: nuclear receptor coactivator 4; FTH1: ferritin, heavy polypeptide 1; GSH: glutathione; MDA: malondialdehyde; SOD: superoxide dismutase. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
Figure 4 Moxibustion attenuates post-MI HF myocardial fibrosis and improves cardiac function A: Masson’s trichrome staining of tissue samples from rats after 8 weeks (scale bar, 50 μm); A1: CON group; A2: MOD group; A3: MOX group; A4: RAPA group; A5: MOX + RAPA group; B: the areas of cardiac fibrosis were quantified by Masson’s trichrome staining; C: representative Western blot bands showing protein expression of cTnT and NT-ProBNP, and β-actin in the myocardium of rats; D: quantitative analysis of cTnT protein expression normalized to β-actin; E: quantitative analysis of NT-ProBNP protein expression normalized to β-actin; F: cTnT mRNA expression levels across experimental groups; G: NT-ProBNP mRNA expression levels across experimental groups. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks; MI: myocardial infarction; HF: heart failure; cTnT: cardiac troponin T; NT-ProBNP: N-terminal prohormone of brain natriuretic peptide. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
Figure 4 Moxibustion attenuates post-MI HF myocardial fibrosis and improves cardiac function A: Masson’s trichrome staining of tissue samples from rats after 8 weeks (scale bar, 50 μm); A1: CON group; A2: MOD group; A3: MOX group; A4: RAPA group; A5: MOX + RAPA group; B: the areas of cardiac fibrosis were quantified by Masson’s trichrome staining; C: representative Western blot bands showing protein expression of cTnT and NT-ProBNP, and β-actin in the myocardium of rats; D: quantitative analysis of cTnT protein expression normalized to β-actin; E: quantitative analysis of NT-ProBNP protein expression normalized to β-actin; F: cTnT mRNA expression levels across experimental groups; G: NT-ProBNP mRNA expression levels across experimental groups. CON: control group; MOD: model group, heart failure after myocardial infarction; MOX: moxibustion group, moxibustion at acupoints Feishu (BL13) and Xinshu (BL15), once daily for 30 min, q.d. 4 weeks; RAPA: rapamycin group, 1 mg/kg, q.d. 4 weeks; MOX + RAPA: moxibustion + rapamycin group, combined moxibustion and rapamycin intervention, q.d. 4 weeks; MI: myocardial infarction; HF: heart failure; cTnT: cardiac troponin T; NT-ProBNP: N-terminal prohormone of brain natriuretic peptide. Data were processed by one-way analysis of variance and values are expressed as mean ± standard deviation (n = 3). Compared with the Control group, aP < 0.01; compared with the Model group, bP < 0.01; compared with the rapamycin group, cP < 0.01.
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