[Electroacupuncture pretreatment alleviated cerebral ischemia-reperfusion injury via suppressing autophagy in cerebral cortex tissue in rats].
Zhen Ci Yan Jiu. 2019 Dec 25 ;44(12):867-72. PMID: 31867904
OBJECTIVE: To investigate the effect of electroacupuncture (EA) preconditioning on autophagy in cerebral cortex tissues of rats with cerebral ischemia-reperfusion injury (CIRI), so as to explore its mechanisms underlying improvement of CIRI.
METHODS: Thirty-three male Sprague-Dawley rats were randomly divided into sham operation, model and EA groups (=11 in each group). EA (2 Hz/15 Hz, 1 mA) was applied to"Baihui"(GV20),"Quchi"(LI11) and"Zusanli"(ST36) for 30 min, once daily for 5 days, followed by establishment of CIRI model by occlusion of the middle cerebral artery (MCAO) for 1.5 h and reperfusion for 24 h. The neurological deficit score was assessed in reference to Longa's methods, and the infarct volume assessed by 2,3,5-triphenyltetrazolium chloride staining. The density of dendrite spines of neurons in the ischemic cerebral cortex tissue was detected by Golgi's staining, the autophagosome observed by electron microscopy, and the expression levels of microtubule-associated protein 1 light chain 3 (LC3) and p62 (a selective autophagy substrate) were detected by Western blot.
RESULTS: Compared with the sham operation group, the neurological deficit score and infarct volume were significantly increased (<0.01), the number of autophagosomes and the ratio of LC3-Ⅱ/LC3-Ⅰ also significantly increased (<0.01), while the expression level of p62 was notably decreased in the model group (<0.01). Following the intervention and in comparison with the model group, the neurological deficit score and infarct volume were significantly reduced (<0.01), the number of autophagosomes and the ratio of LC3-Ⅱ/LC3-Ⅰ obviously decreased (<0.01), and the expression of p62 was significantly up-regulated in the EA group (<0.01).
CONCLUSION: EA pretreatment is effective in improving CIRI in rats, which may be realized through suppressing autophagy in the ischemic cerebral cortex tissue.