Abstract: OBJECTIVE  To investigate the effects of electroacupuncture (EA) pretreatment on cardiac dysfunction and inflammatory reaction in lipopolysaccharide (LPS)induced sepsis mice, and to explore the possible mechanisms of EA preconditioning for cardioprotection.METHODS  A total of 24 male C57BL/6J mice were randomized into 3 groups: control group, model group, and EA pretreatment group, with 8 mice in each group. Before modeling, mice in the EA pretreatment were given "Zusanli" (ST36) EA stimulation (2/15 Hz, 2 mA, 15 min)under anesthesia with isoflurane. The model group and the control group were only fixed for 15 min in the same way. The sepsis mice models were established by intraperitoneal injection of LPS (10 mg/kg). Similar to the control group, an equal volume of saline was administered. Cardiac function was measured by echocardiography and the contents of inflammatory cytokines in serum was examined by ELISA. The mRNA and protein expression levels of inflammatory cytokines in cardiac tissue were detected with qPCR and Western blot respectively, the number of F4/80⁺CD11b⁺macrophages and the contents of F4/80⁺CD11b⁺CD206^low M1 and F4/80⁺CD11b⁺CD206^high M2 macrophages in myocardium was determined by flow cytometry.RESULTS  Compared with the control group, the LVEF, LVFS value of the model group was decreased (P < 0.01), the serum levels of TNF-α, IL-1β increased (P < 0.01), the expression of TNF-α, IL-1β, IL-6, IL-10 mRNA and protein increased (P < 0.01, P < 0.05), the number of F4/80⁺CD11b⁺macrophages in cardiac tissue increased (P < 0.01), the proportion of F4/80⁺CD11b⁺CD206^low M1 macrophages increased (P < 0.01). Nevertheless, EA pretreatment group could reverse these changes mentioned above in the model group. Compared with the model group, the LVEF, LVFS values increased significantly (P < 0.01), the serum levels of TNF-α, IL-1β decreased (P < 0.05, P < 0.01), the expression of pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and the number of macrophages in the myocardium downregulated (P < 0.05, P < 0.01), the expression of anti-inflammatory interleukins IL-10 (P < 0.05) and the proportion of M2 macrophages in the myocardium upregulated (P < 0.01).CONCLUSION  EA preconditioning may promote the polarization of macrophages in myocardial tissue from M1 pro-inflammatory macrophages to M2 anti-inflammatory macrophages, reduce the level of systemic and local inflammation, improve heart function, and produce myocardial protection.