Objectives: Previous studies have shown that cannabinoid receptor type 2 (CB2R) is activated in a pilocarpine-induced SE model of SD rats,and kept the same pace with neuronal autophagy. Therefore, the purpose of this study is intended to explore the relationship between CB2R and autophagy in neuronal repair process in pilocarpine-induced status epilepticus rats, and the mechanism.

Methods: A total of 80 health male Sprague-Dawley rats, aging 3 weeks, were divided into Vehicle group、Epilepsy group、JWH133(CB2R agonist) 1ug/ul group、JWH133 3ug/ul group and JWH133+AM630(CB2R antagonist) group treated by intracerebroventricular injection at 60min before modeling.At 24h after SE, the apoptosis of neurons in hippocampal tissue was observed by HE staining and TUNEL staining.The expression of LC3 and mTOR were observed by double-immunoinfluorescence staining. The expression of mTOR、p-mTOR、ULK1、p-ULK1、Beclin1、LC3、p62 were observed by western blot.

Results: Compared with rats in the Vehicle group, the expression of p-mTOR/mTOR、Beclin1、LC3Ⅱ/LC3Ⅰ were increased in the JWH133 group at 1 day post-SE(p＜0.05), while p-ULK1/ ULK1、p62和Caspase-3 were decreased in the JWH133 group at 1 day post-SE(p＜0.05),the effect was weaken when was added with AM630 and JWH133 simultaneously at 1 day post-SE(p＜0.05).

Conclusions: The autophagy after SE was inforced by activation of CB2R, and the apoptosis was wakened accordingly. Effects of CB2R on hippocampal neuronal autophagy come to ture through mTOR signaling pathway. CB2R is a potent target in the early stage of neutonal repair after SE.