Table 2.

Summary of intervention parameters of EA pretreatment against MIRI in animal experiments.

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