| Reference | EA pretreatment | Mechanisms | ESP | Acupoint |
| Gao et al., 2006 [22] | 20 Hz, 5 mA, 30 min, 3 days | Neiguan acupoint (PC6) | β-Adrenoceptors was involved | Huang et al., 2014 [24] | 2/15 Hz, 1 mA, 20 min, 12 days, a day of rest after six days | Neiguan acupoint (PC6) | These genes were involved in multiple pathways, including ECM, MAPK signaling, apoptosis, cytokine, and leukocyte pathways; in addition, some pathways were uniquely regulated by EA, such as oxidative stress, cardiac muscle contraction, gap junction, vascular smooth muscle contraction, hypertrophic, NOD-like receptor, P53, and B-cell receptor pathways | Gao et al., | | | | 2015 [28] | 20 Hz, 1–3 mA, 30 min, 3 days | Neiguan acupoint (PC6) | EA pretreatment could inhibit SGIR-induced calcium overload and [Ca2+]i oscillations, reduce nonphosphorylated Cx43, and enhance the corresponding phosphorylated Cx43 in the cardiac cells | Shao et al., 2017 [29] | 2–100 Hz, 1 mA, 30 min, 7 days | Jiaji T4∼T5 acupoint (EX-B2), Neiguan acupoint (PC 6), and Quchi acupoint (LI 11) | Acupuncture pretreatment at “Jiaji” (EX-B2) had the protective effect on MIRI, which was probably relevant with the upregulation of Nrf 2-ARE pathway expression, the activation of the endogenous antioxidative pathway, the improvement of oxygen free radical scavenging capacity, and the alleviation of lipid peroxide damage | Wang et al., 2014 [30] | 20 min, 5 days | Neiguan acupoint (PC6) | Acupuncture and moxibustion pretreatment may suppress MIRI-induced increase of plasma ET and serum CK and upregulate myocardial HSP 70 protein expression in MIRI rabbits |
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