Details

Autor(en) / Beteiligte

• Jing, Xin-yue
• Zhu, Bing-Mei
• Chen, Xia
• Yu, Mei-ling
• Li, Qian
• Fu, Shu-ping
• Shen, Weixing
• Wang, Ning
• Huang, Yan
• Lu, Sheng-feng
• Liu, Wan-xin
• Hsieh, Ching-Liang

Titel

Cardioprotective Effect of Electroacupuncture Pretreatment on Myocardial Ischemia/Reperfusion Injury via Antiapoptotic Signaling

Ist Teil von

• Evidence-based complementary and alternative medicine, 2016-01, Vol.2016 (2016), p.1-9

Ort / Verlag

Cairo, Egypt: Hindawi Publishing Corporation

Erscheinungsjahr

2016

Quelle

Electronic Journals Library

Beschreibungen/Notizen

• Objectives. Our previous study has used RNA-seq technology to show that apoptotic molecules were involved in the myocardial protection of electroacupuncture pretreatment (EAP) on the ischemia/reperfusion (I/R) animal model. Therefore, this study was designed to investigate how EAP protects myocardium against myocardial I/R injury through antiapoptotic mechanism. Methods. By using rats with myocardial I/R, we ligated the left anterior descending artery (LAD) for 30 minutes followed by 4 hr of reperfusion after EAP at the Neiguan (PC6) acupoint for 12 days; we employed arrhythmia scores, serum myocardial enzymes, and cardiac troponin T (cTnT) to evaluate the cardioprotective effect. Heart tissues were harvested for western blot analyses for the expressions of pro- and antiapoptotic signaling molecules. Results. Our preliminary findings showed that EAP increased the survival of the animals along with declined arrhythmia scores and decreased CK, LDH, CK-Mb, and cTnT levels. Further analyses with the heart tissues detected reduced myocardial fiber damage, decreased number of apoptotic cells and the protein expressions of Cyt c and cleaved caspase 3, and the elevated level of Endo G and AIF after EAP intervention. At the same time, the protein expressions of antiapoptotic molecules, including Xiap, BclxL, and Bcl2, were obviously increased. Conclusions. The present study suggested that EAP protected the myocardium from I/R injury at least partially through the activation of endogenous antiapoptotic signaling.