查看更多>>摘要:Objective:To explore the mechanism of electroacupuncture(EA)in promoting recovery of the facial function with the involvement of autophagy,glial cell line-derived neurotrophic factor(GDNF),and phosphatidylinositol-3-kinase(PI3K)/mammalian target of rapamycin(mTOR)signaling pathway.Methods:Seventy-two male Sprague-Dawley rats were randomly allocated into the control,sham-operated,facial nerve injury(FNI),EA,EA+3-methyladenine(3-MA),and EA+GDNF antagonist groups using a random number table,with 12 rats in each group.An FNI rat model was established with facial nerve crushing method.EA intervention was conducted at Dicang(ST 4),Jiache(ST 6),Yifeng(SJ 17),and Hegu(LI 4)acupoints for 2 weeks.The Simone's 10-Point Scale was utilized to monitor the recovery of facial function.The histopathological evaluation of facial nerves was performed using hematoxylin-eosin(HE)staining.The levels of Beclin-1,light chain 3(LC3),and P62 were detected by immunohistochemistry(IHC),immunofluorescence,and reverse transcription-polymerase chain reaction,respectively.Additionally,IHC was also used to detect the levels of GDNF,Rai,PI3K,and mTOR.Results:The facial functional scores were significantly increased in the EA group than the FNI group(P<0.05 or P<0.01).HE staining showed nerve axons and myelin sheaths,which were destroyed immediately after the injury,were recovered with EA treatment.The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats(P<0.01);however,EA treatment reversed these abnormal changes(P<0.01).Meanwhile,EA stimulation significantly increased the levels of GDNF,Rai,PI3K,and mTOR(P<0.01).After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist,the repair effect of EA on facial function was attenuated(P<0.05 or P<0.01).Conclusions:EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI.EA may exert this neuroreparative effect through mediating the release of GDNF,activating the PI3K/mTOR signaling pathway,and further regulating the autophagy of facial nerves.