Yang Lou ,
Bo Xu,
Xianshuai Li,
Xiaoyi Xu,
Xiaoguo Chen
Department of Cardiothoracic Surgery, Jinhua Municipal Central Hospital, No. 365 Renmin East Road, Jinhua, Zhejiang 321000, China;
For correspondence:- Yang Lou
Email: uoyangjinhua12@163.com Tel:+8657982552611
Accepted: 24 December 2019
Published: 31 January 2020
Citation:
Lou Y, Xu B, Li X, Xu X, Chen X.
Schisandra chinensis extract ameliorates myocardial ischemia/reperfusion injury via TLR4/NF-κB/MyD88 signaling pathway. Trop J Pharm Res 2020; 19(1):57-62
doi:
10.4314/tjpr.v19i1.9
© 2020 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..
Abstract
Purpose: To investigate the effects of Schisandra chinensis extract (SCE) on myocardial ischemia-reperfusion (I/R) injury and to elucidate its underlying mechanism of action.
Methods: A rat model of myocardial I/R injury was used. Ischemia was induced by occluding the left anterior descending artery for 30 min and the myocardium was then reperfused for 2 h in Sprague-Dawley rats. Triphenyltetrazolium chloride (TTC) staining was used to measure myocardial infarct size, while the levels of inflammatory cytokines were evaluated by enzyme-linked immunosorbent assay (ELISA). Western blot assay was conducted to determine protein levels.
Results: TTC staining showed that myocardial I/R injury was ameliorated after SCE treatment. Serum creatine kinase (CK), lactate dehydrogenase (LDH), and malondialdehyde (MDA) levels decreased, whereas superoxide dismutase (SOD) activity increased after SCE treatment. Moreover, serum interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) expression levels were reduced after SCE treatment. Furthermore, SCE treatment remarkably downregulated the protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor-kappa B (NF-κB), and myeloid differentiation factor 88 (MyD88).
Conclusion: SCE may exert protective effects against myocardial I/R injury by downregulating TLR4-mediated NF-κB/MyD88 signaling pathway. However, this needs to confirmed in clinical studies.
Keywords: Schisandra chinensis, TLR4/NF-_4;B/MyD88, In@258;ammasome, Myocardial ischemia-reperfusion injury