Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in MiceReport as inadecuate




Ginsenoside Rb1 Treatment Attenuates Pulmonary Inflammatory Cytokine Release and Tissue Injury following Intestinal Ischemia Reperfusion Injury in Mice - Download this document for free, or read online. Document in PDF available to download.

Oxidative Medicine and Cellular Longevity - Volume 2015 2015, Article ID 843721, 12 pages -

Research Article

Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan 430060, China

Department of Cardiovascular Surgery, Renmin Hospital of Wuhan University, Wuhan 430060, China

Department of Anesthesiology, The University of Hong Kong, Pok Fu Lam, Hong Kong

Department of Anesthesiology, Affiliated Hospital of Guangdong Medical College, Zhanjiang, Guangdong 524001, China

Received 18 September 2014; Revised 22 December 2014; Accepted 27 December 2014

Academic Editor: Yanfang Chen

Copyright © 2015 Ying Jiang et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective. Intestinal ischemia reperfusion II-R injury plays a critical role in remote organ dysfunction, such as lung injury, which is associated with nuclear factor erythroid 2-related factor 2 Nrf2-heme oxygenase-1 HO-1 signaling pathway. In the present study, we tested whether ginsenoside Rb1 attenuated II-R induced lung injury by Nrf2-HO-1 pathway. Methods. II-R injury was induced in male C57BL-6J mice by 45 min of superior mesenteric artery SMA occlusion followed by 2 hours of reperfusion. Ginsenoside Rb1 was administrated prior to reperfusion with or without ATRA all-transretinoic acid, the inhibitor of Nrf2-ARE signaling pathway administration before II-R. Results. II-R induced lung histological injury, which is accompanied with increased levels of malondialdehyde MDA, interleukin- IL- 6, and tumor necrosis factor- TNF- α but decreased levels of superoxide dismutase SOD and IL-10 in the lung tissues. Ginsenoside Rb1 reduced lung histological injury and the levels of TNF-α and MDA, as well as wet-dry weight ratio. Interestingly, the increased Nrf2 and HO-1 expression induced by II-R in the lung tissues was promoted by ginsenoside Rb1 treatment. All these changes could be inhibited or prevented by ATRA. Conclusion. Ginsenoside Rb1 is capable of ameliorating II-R induced lung injuries by activating Nrf2-HO-1 pathway.





Author: Ying Jiang, Zhen Zhou, Qing-tao Meng, Qian Sun, Wating Su, Shaoqing Lei, Zhengyuan Xia, and Zhong-yuan Xia

Source: https://www.hindawi.com/



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