基于AMPK/mTOR/Ulk1信号通路探讨电针干预颅脑损伤模型大鼠的作用机制OA

Objective To investigate the effect of electroacupuncture(EA)intervention on behavior,hippocampal neuron morphology,and adenosine monophosphate-activated protein kinase(AMPK)/mammalian target of rapamycin(mTOR)/Unc-51 like autophagy acti-vating kinase 1(Ulk1)signaling pathway-mediated autophagy and apoptosis in a unilateral traumatic brain injury(TBI)rat model.Methods One hundred specific pathogen-free(SPF)male Sprague-Dawley(SD)rats were randomly divided into the blank group(n=10),sham-operated group,model group,and EA group(n=30 each).The latter three groups were further divided into three subgroups(n=10 each)according to observation time points(3,7,14 days).A TBI model was established using the modified Feeney's weight-drop method.The EA group received treatment at Baihui(GV 20),Guanyuan(CV 4),Quchi(LI 11),and Hegu(LI 4)acupoints for 15 min daily,starting 24 h post-surgery for 14 consecutive days.Neurological deficits were assessed using modified neurological sever-ity score(mNSS).Apoptosis was detected by TUNEL staining.Protein and mRNA expression of AMPK,mTOR,and Ulk1 were mea-sured by Western blot(WB)and quantitative real-time PCR(qRT-PCR),respectively.Results Compared with the sham-operated group,the model group showed significantly increased mNSS scores,apoptosis mean optical density values,and phosphorylated AMPK and Ulk1 protein and mRNA expression at all time points(P<0.01).Compared with the model group,the EA group exhibited decreased mNSS scores,apoptosis mean optical density values,and phosphorylated mTOR protein and mRNA expression at all interven-tion time points(P<0.05).Conclusion EA intervention may inhibit excessive cellular autophagy and reduce apoptosis by regulating the AMPK/mTOR/Ulk1 signaling pathway,thereby promoting neurological functional recovery in unilateral TBI model rats.