Electroacupuncture at Quchi and Zusanli points reduces cell apoptosis by activating Nrg-1 and ErbB4 signaling pathways in cerebral ischemia-reperfusion rats / 医学研究生学报

ABSTRACT

Objective The mechanism of electroacupuncture (EA) in the treatment of neurological dysfunction caused by ischemic stroke remains to be further explored. This study aimed to investigate the effects of EA at the Quchi (LI11) and Zusanli (ST36) points on the expressions of Nrg-1 and ErbB4 proteins and their correlation with the expressions of cell apoptosis-related proteins bcl-2 and Bax in cerebral ischemia-reperfusion (I-R) rats.Methods Totally 160 male adult SD rats were randomly assigned to four groups of equal number sham operation, middle cerebral artery occlusion-reperfusion (MCAO-R) model, acupoint, and non-acupoint. After MCAO/R modeling, EA was applied at Quchi and Zusanli in the acupoint group and at ipsilateral non-acupoints below the axillary striation and apex of the coccyx in the non-acupoint group. At 3 days after treatment, the protein and mRNA expressions of Bcl-2, Bax, Nrg-1 and ErbB4 were determined by TTC, TUNEL, immunohistochemistry, Western blot, and RT-PCR.Results The neurological deficit score was significantly increased after cerebral I/R injury in the MCAO-R model, acupoint and non-acupoint groups compared with that in the sham operation group (P<0.01). EA therapy markedly reduced the neurological deficit scores (P<0.05), cerebral infarct area (P<0.05) and the number of apoptotic cells (P<0.05), up-regulated the protein expressions of Nrg-1, ErbB4 and Bcl-2 (P<0.05), and down-regulated that of Bax (P<0.05). There was a pronounced increase in the protein and mRNA expressions of Nrg-1 and ErbB4 in the acupoint group compared with the MCAO-R model and non-acupoint groups after cerebral I-R injury (P<0.01).Conclusion EA at the Quchi and Zusanli points has a neuroprotective effect in ischemic brain injury by up-regulating the expressions of endogenous Nrg-1 and its receptor ErbB4 and down-regulating those of Bcl-2 and Bax. The underlying mechanism is probably associated with the Nrg-1/ErbB4 signaling pathway.