Purpose: The objective of this study was to investigate the mechanism of electroacupuncture pretreatment in reducing myocardial ischemia-reperfusion injury in rats.
Materials and methods: The comparison of HR among the different groups did not yield statistically significant differences (p > 0.05). Additionally, the trend of HR change at different time points within each group was not statistically significant (p > 0.05). In contrast, the comparison of SBP among the different groups showed statistically significant differences (p < 0.05). Furthermore, the trend of SBP change at different time points within each group exhibited significant differences (p < 0.05).
Results: Compared to the Sham group, rats in the I/R group and EA control group showed a significant decrease in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and an increase in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05). Compared to EA control group, rats in the EA group exhibited a significant increase in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and a decrease in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05). Compared to the EA group, rats in the EA + RAP group showed a significant decrease in EF, FS, SOD, p-mTOR/mTOR, GPX4, and FTH1, and an increase in CK-MB, cTnI, LDH, iron, ROS, MDA, ACSL4, and NCOA4 (p < 0.05).
Conclusions: Electroacupuncture preconditioning confers protective effects against myocardial ischemia-reperfusion injury in rats. Its mechanism may involve the activation of the mTOR/ROS signaling pathway by electroacupuncture to inhibit ferroptosis.
Keywords: Electroacupuncture; ferroptosis; iron autophagy; iron death; lipid peroxides; mTOR/ROS; myocardial ischemia-reperfusion injury.