[Effect of electroacupuncture on expression of corticocerebral autophagy-related proteins in rats with traumatic brain injury].

Objective: To observe the effect of electroacupuncture on the expression of phosphorylated adenosine 5'-monophosphate-activated protein kinase(p-AMPK), phosphorylated mammalian target of rapamycin(p-mTOR) and phosphorylated Ulk1(p-Ulk1) proteins in the cortex of traumatic brain injury (TBI) rats, so as to explore its mechanisms underlying treatment of TBI.

Methods: Male SD rats were randomly divided into sham operation (sham), model, electroacupuncture Ⅰ (EA Ⅰ), electroacupuncture Ⅱ (EA Ⅱ) groups (＝10 in each group). TBI model was established by using a free fall brain injury striking device after exposing the local cranial bone (to induce the left parietal cerebral contusion). Rats in EA Ⅰ group were treated by electroacupuncture at "Neiguan" (SP6) and "Zusanli" (ST36) combined with acupuncture at "Shuigou" (GV26) and "Baihui"(GV20) on the 7day after modeling, once a day for 7 consecutive days. Rats in EA Ⅱ group received the treatments as those in EA Ⅰ group on 24 h after modeling, once a day for 14 d. After the treatment, histopathological changes of the injured cerebral cortex were observed by HE staining and Nissl staining. Western blot was used to detect the expression of AMPK, p-AMPK, mTOR, p-mTOR, Ulk1, p-Ulk1 proteins in the injured cerebral cortex tissue.

Results: After modeling and compared with the sham group, a large number of tissue necrosis, scattered arrangement of nerve fibers, vacuolar changes of cells, nuclear fragmentation, consolidation and hyperplastic scar tissue were found in the brain trauma area of rats in the model group. Nissl corpuscles were obviously absent. The ratio of p-AMPK/AMPK was up-regulated in the cortex of the wound region (<0.01), and the ratio of p-mTOR/mTOR, p-Ulk1/Ulk1 were down-regulated (<0.01). Compared with the model group, the pathological changes in brain injury area of rats in both EA groups were alleviated, the number of Nissl corpuscles increased, the ratio of p-AMPK/ AMPK was down-regulated in cortex of the injury area (<0.01), and the ratios of p-mTOR/mTOR and p-Ulk1/Ulk1 were up-regulated (<0.01). Compared with EA Ⅰ group, the pathological changes in the brain injury area in EA Ⅱ group showed obvious improvement, with down-regulation of p-AMPK/AMPK (<0.05), and up-regulation of p-mTOR/mTOR and p-Ulk1/Ulk1 (<0.05).

Conclusion: Electroacupuncture may inhibit the over-activation of autophagy of cranial neurons by regulating the activation of AMPK, mTOR and Ulk1, thus exerting brain protection effect on TBI rats, and early electroacupuncture intervention is more effective in acute phase of TBI.