Key result
Moxibustion improves post-ischemia LVEF to ~65% vs. 47% in reperfused rat models.
Why the study?
Whether moxibustion preserves the structural integrity essential for mitochondrial function in myocardial ischemia-reperfusion injury remains unknown, prompting investigation into cardiolipin as a novel target of cardioprotection.
Does moxibustion improve cardiac function and reduce pathological remodeling in a rat model of myocardial ischemia-reperfusion injury?
Does moxibustion improve cardiac function and reduce pathological remodeling in a rat model of myocardial ischemia-reperfusion injury?
Absolute Event Rate: 65.2% vs 47%
p-value: p=<0.0001
Moxibustion attenuates myocardial ischemia-reperfusion injury and pathological remodeling in rats by preserving mitochondrial cardiolipin via the AMPK-oxidative stress axis.
Hypothesis-generating for moxibustion in myocardial ischemia-reperfusion injury; leaves open translation to human cardiac therapy.
Objective: Moxibustion has been shown to protect against myocardial ischemia-reperfusion injury (MIRI) by regulating mitochondrial function. Whether it preserves the structural integrity essential for this function remains unknown. Based on the critical role of cardiolipin (CL) in mitochondrial membranes, this study aimed to investigate whether CL serves as a novel target of moxibustion-mediated cardioprotection. Methods and results: A rat model of MIRI was established by ligating the left anterior descending (LAD) coronary artery for 30 min followed by 7 days of reperfusion. Moxibustion was applied to Neiguan acupoint (PC6) every other day during reperfusion. Moxibustion exerted significant cardioprotective effects by reducing interstitial fibrosis, alleviating cardiac hypertrophy, and improving cardiac function. Mechanistically, moxibustion attenuated oxidative stress-mediated mitochondrial injury, as shown by decreased ROS, 4-hydroxynonenal (4-HNE), total oxidative status (TOS), and oxidative stress index (OSI) levels, increased total antioxidant capacity (TAC), and preserved mitochondrial cristae structure. Moreover, moxibustion restored total CL levels, concomitant with downregulation of Acyl-CoA:lysocardiolipin acyltransferase-1 (ALCAT1) and reduction of cytosolic cytochrome c (Cyt c). Moxibustion also upregulated AMP-activated protein kinase (AMPK) phosphorylation, an effect reversed by Compound C which also largely abolished the cardioprotective effects, suggesting AMPK involvement. Conclusion: This study provides evidence for the involvement of the AMPK-oxidative stress-CL axis in moxibustion-mediated cardioprotection, highlighting the potential of moxibustion as a non-pharmacological intervention for ischemic heart disease.
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Chunmei et al. (2026) studied Myocardial ischemia-reperfusion injury (MIRI) (n=45). Moxibustion vs. MIRI model without moxibustion was evaluated on Left ventricular ejection fraction (LVEF) at 7 days (p=<0.0001). Moxibustion significantly improved cardiac function in rats with myocardial ischemia-reperfusion injury, increasing left ventricular ejection fraction to 65.20% compared to 47.00% in untreated controls.
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