Picroside Ⅱ protects myocardium from ischemia/reperfusion‑induced injury through inhibition of the inflammatory response

Li,Jian‑Zhe; Xie,Mei‑Qing; Mo,Dan; Zhao,Xiao‑Fang; Yu,Shu‑Yi; Liu,Li‑Juan; Wu,Cheng; Yang,Yang

doi:10.3892/etm.2016.3841

Picroside Ⅱ protects myocardium from ischemia/reperfusion‑induced injury through inhibition of the inflammatory response

Authors:
- Jian‑Zhe Li
- Mei‑Qing Xie
- Dan Mo
- Xiao‑Fang Zhao
- Shu‑Yi Yu
- Li‑Juan Liu
- Cheng Wu
- Yang Yang
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Affiliations: Department of Pharmacy, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China, Department of Hepatobiliary, Glandular and Peripheral Vascular Surgery, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China, Department of Surgery, Maternal and Child Health Hospital of The Guangxi Zhuang Autonomous Region, Nanning, Guangxi 530003, P.R. China, Department of Liver Diseases, Ruikang Hospital, Guangxi University of Chinese Medicine, Nanning, Guangxi 530011, P.R. China, Advanced Research Center, Central South University, Changsha, Hunan 410078, P.R. China, Department of Pharmacy, Jiangxi Provincial Cancer Hospital, Nanchang, Jiangxi 330029, P.R. China
Published online on: October 26, 2016 https://doi.org/10.3892/etm.2016.3841
Pages: 3507-3514
Copyright: © Li et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R‑induced injury, however, the exact mechanism underlying these protective effects remains unclear. The aim of the present study was to investigate the mechanism underlying the protective effects of picroside II on I/R‑induced myocardial injury. Adult male Sprague‑Dawley rats underwent 1 h left coronary artery occlusion followed by 3 h reperfusion. Picroside II was administered (10 mg/kg) via the tail vein 30 min prior to left coronary artery occlusion. The results revealed that pretreatment of picroside II could significantly alleviate I/R‑induced myocardial injury concomitantly with a decrease in inflammatory factor production. In addition, picroside II was also able to decrease high mobility group box 1 (HMGB1) expression, and release and downregulate the expression of the receptor for advanced glycation end products (RAGE), toll‑like receptor (TLR)‑2 and TLR‑4. Furthermore, picroside II was able to inhibit nuclear factor‑κB (NF‑κB) activation. The results indicated that the protective effect of picroside II on I/R‑induced myocardial injury was associated, at least partly, with inhibition of the inflammatory response by suppressing the HMGB1‑RAGE/TLR‑2/TLR‑4‑NF‑κB signaling pathway.

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