Electroacupuncture Promotes Neural Cell Proliferation In Vivo Through Activation Of ERk1/2Signaling Pathway

Objectives: The aim of this study was to investigate whether mediated ERK1/2signal transduction pathways involved in cell proliferation by electroacupuncturing at acupoints of Zusanli(ST36) and Quchi(LIll). thus protecting cerebral ischemia-reperfusion injury. Methods:100rats were randomly divided into5groups:sham operation control (SC). ischemia control (IC). EA. EA and DMSO injection (ED). EA and U0126injection (EU) each group20rats. All groups but SC were performed with middle cerebral artery occlusion (MCAO), DMSO or U0126was injected into the rat in ED or EU group30min before MCAO. Neurological deficit scores (NDSs) were performed once a day2h after ischemia-reperfusion. On the first day after MCAO, the electroacupuncture was performed for30min once per day. and the rats were killed after3days electroacupuncture. The change of cerebral infarction volume was examined by TTC staining. Cell proliferation was evaluated by PCNA immunostaining. The changes of cell cycle proteins (cyclin Dl, CDK4, cyclin E, CDK2, p21and p27) and ERKl/2pathway activation were examined by RT-PCR and western blot. Results:3days after electroacupuncture. the NDSs in EA and ED groups showed significant difference compared to IC group (P<0.05). but there was no obvious difference between IC and EU. and between EA and ED as well (P>0.05). The positive cell numbers of PCNA immunstaining shown were much less in other four groups compared with SC group, among four groups, the positive cell numbers in EA and ED groups were more than that in IC group (P<0.05). The results from RT-PCR and western blot showed that mRNA and protein levels of p21or p27were obviously increased, but mRNA and protein levels of cyclin Dl. CDK4. cyclin E and CDK2were reduced in IC and EU groups. Conclusion: The electroacupuncture activates the ERK1/2signaling pathway to activate downstream transcription factors including cyclin D1. CDK4. cyclin E and CDK2, and thus promotes the process of the Gl to S phase to protect brain injury during cerebral ischemia.