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Previous studies found that electroacupuncture (EA) at the Shenting (DU24) and Baihui (DU20) acupoints alleviates cognitive impairment in cerebral ischemia-reperfusion (I/R) injury rats. Nonetheless, the mechanisms of the anti-inflammatory effects of EA are unclear. Cerebral I/R injury was induced in rats by middle cerebral artery occlusion (MCAO). Following I/R injury, the rats underwent EA therapy at the Shenting (DU24) and Baihui (DU20) acupoints for seven successive days. The Morris water maze test, magnetic resonance imaging (MRI) and molecular biology assays were utilized to assess the establishment of the rat stroke model with cognitive impairment and the therapeutic effect of EA. EA treatment of rats subjected to MCAO showed a significant reduction in infarct volumes accompanied by cognitive recovery, as observed in Morris water maze test outcomes. The possible mechanisms by which EA treatment attenuates cognitive impairment are by regulating endogenous melatonin secretion through aralkylamine N-acetyltransferase gene (AANAT, a rate-limiting enzyme of melatonin) synthesis in the pineal gland in stroke rats. Simultaneously, through melatonin regulation, EA exerts neuroprotective effects by upregulating mitophagy-associated proteins and suppressing reactive oxygen species (ROS)-induced NLRP3 inflammasome activation after I/R injury. However, melatonin receptor inhibitor (luzindole) treatment reversed these changes. The findings from this research suggested that EA ameliorates cognitive impairment through the inhibition of NLRP3 inflammasome activation by regulating melatonin-mediated mitophagy in stroke rats., (© 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

ObjectiveThe purpose of this study is to explore the mechanism of electroacupuncture at Baihui and Shenting acupoints to alleviate cerebral ischemia-reperfusion injury by regulating BNIP3L-mediated mitophagy.MethodsA total of 60 SD rats were randomly divided into sham operation group (n=15) and operation group (n=45) by using the random number table method. Only the blood vessels were separated and exposed in the sham operation group, without ligation and no nylon thread inserted. The rats in the operation group were treated with the middle cerebral artery occlusion (MCAO) method to prepare the focal cerebral ischemia-reperfusion (I/R) model, and the Zea Longa method was used to score the neurological function 2h after the operation. Finally, 30 rats were included in the operation group. The included operation group rats were further randomly divided into the model group, electroacupuncture group, and electroacupuncture+3-MA group, with 10 rats in each group. After grouping, each group was treated with different methods such as electroacupuncture for 7 days, and the Zea Longa method was used to evaluate the neurological function again on the 1, 3, 5, and 7 days. After 7 days of intervention, the left cerebral cortex tissue of each group was obtained, hematoxylin-eosin (HE) staining was used to observe the pathological changes of the brain tissue, the expression level of LC3-Ⅱ/LC3-Ⅰ protein was detected by Western blot, and the tissue immunofluorescence technology was applied to detect the expression and colocalization of mitophagy-related protein BNIP3L and SQSTM1 labeled. The TUNEL method detected the apoptosis rate of rat nerve cells in each group.Results1) The neurological scores of the rats in the operation group were significantly increased 2 hours after the MCAO, and the rats in the sham-operation group did not show symptoms of neurological deficit. On the 7th day after the intervention, the neurological scores of the rats in the model group and the electroacupuncture+3-MA group still increased significantly, which were significantly different from those in the sham operation group (PPPPPP