Abstract

In this study, we investigated the molecular mechanisms underlying the anti-apoptotic properties of electroacupuncture (EA) in a rat model of middle cerebral artery occlusion (MCAO). Treatment with 2Hz EA (1mA) resulted in a markedly reduced infarct area after stroke, particularly in the middle region of the brain. Treatment with EA resulted in a significant decrease in the number of apoptotic cells identified by Hoechst33342 and TUNEL staining. According to the results of the analysis for proteins involved in apoptosis, treatment with EA resulted in a significantly reduced expression of death receptor (DR)5. Among the members of the Bcl‑2 family, a higher expression of anti-apoptotic Bcl‑2 and Bcl‑xL was observed in the rats treated with EA, compared with the untreated rats with MCAO. As regards the expression of the inhibitor of apoptosis protein (IAP) family, a higher expression of anti-apoptotic cIAP‑1 and ‑2 was also detected in the cortex of the EA‑treated rats. Using western blot analysis, we observed that activated caspase‑3 was only significantly arrested by EA treatment in the rats with MCAO; however, according to the results of the caspase assay, the activities of caspase‑3, ‑8 and‑9 were markedly inhibited by EA treatment. These results suggest that treatment with EA exerts anti‑apoptotic effects in cerebral ischemia in a rat model of MCAO and that these effects are associated with the inhibition of the DR and mitochondrial apoptotic pathways.

Full Text
Paper version not known

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.