RESUMO
OBJECTIVE: To explore the effect of electroacupuncture (EA) at "Shuigou"(GV6) and "Baihui"(GV20) on autophagy of hippocampal neurons in cerebral ischemia-reperfusion (I/R) injury rats. METHODS: Forty-eight healthy male SD rats were randomly divided into sham operation, model and EA groups, with 16 rats in each group. The rat model of cerebral I/R injury was established by occlusion of the middle cerebral artery (MCAO). Rats of the EA group received EA at GV26 and GV20 for 20 min, once daily for 5 days. The neurological function of rats in each group was evaluated by Longa neurological function score. The cerebral infarction volume was measured by TTC staining. The levels of IL-6, IL-18 and TNF-α in cerebrospinal fluid were detected by ELISA. Real-time PCR and Western blot were respectively used to detect the expressions of autophagy-related proteins AMPK, Beclin-1, VPS34 and LC3B. RESULTS: Compared with the sham operation group, neurological function scores of rats in the model group were significantly increased (P<0.01); the volume of cerebral infarction was significantly increased (P<0.01); the contents of IL-6, IL-18 and TNF-α in cerebrospinal fluid were increased (P<0.01, P<0.05); the mRNA expression levels of AMPK, Beclin-1, VPS34 and LC3B were significantly increased (P<0.01); the protein expressions of AMPK, Beclin-1, VPS34 and the ratio of LC3B-â ¡/LC3B-â were increased (P<0.01, P<0.05). After intervention and in comparison with the model group, the neurological function scores were decreased (P<0.05); the cerebral infarct volume were decreased (P<0.05); the contents of IL-6, IL-18 and TNF-α in cerebrospinal fluid were decreased (P<0.05); the mRNA expressions of AMPK, Beclin-1, VPS34 and LC3B were significantly decreased (P<0.01); the protein expressions of AMPK, Beclin-1, VPS34 and the ratio of LC3B-â ¡/LC3B-â were decreased (P<0.05, P<0.01). CONCLUSION: EA can improve the neurological function and alleviate the degree of nerve injury in rats with cerebral I/R injury, which may be related to inhibiting the autophagy level of hippocampal neurons.