Effects of electroacupuncture on apoptotic pathways in a rat model of focal cerebral ischemia

Kim,Yu Ri; Kim,Ha  Neui; Jang,Ji  Yeon; Park,Cheol; Lee,Jun  Hyuk; Shin,Hwa   Kyoung; Choi,Yung  Hyun; Choi,Byung  Tae

doi:10.3892/ijmm.2013.1511

Effects of electroacupuncture on apoptotic pathways in a rat model of focal cerebral ischemia

Authors:
- Yu Ri Kim
- Ha Neui Kim
- Ji Yeon Jang
- Cheol Park
- Jun Hyuk Lee
- Hwa Kyoung Shin
- Yung Hyun Choi
- Byung Tae Choi
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Affiliations: Division of Meridian and Structural Medicine, School of Korean Medicine, Pusan National University, Yangsan 626-870, Republic of Korea, Department of Biochemistry, College of Oriental Medicine, Anti-Aging Research Center and Blue-Bio Industry RIC, Dongeui University, Busan 614-052, Republic of Korea, Chemistry and Biotechnology Examination Bureau, Korean Intellectual Property Office, Daejeon 302-701, Republic of Korea
Published online on: September 27, 2013 https://doi.org/10.3892/ijmm.2013.1511
Pages: 1303-1310

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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 2 Hz EA (1 mA) 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 Hoechst 33342 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.

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