Galuteolin attenuates cerebral ischemia/reperfusion injury in rats via anti-apoptotic, anti-oxidant, and anti-inflammatory mechanisms
Authors Cheng X, Zhang F, Li J, Wang G
Received 10 May 2019
Accepted for publication 3 August 2019
Published 16 September 2019 Volume 2019:15 Pages 2671—2680
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Jun Chen
Xue Cheng,1 Fan Zhang,1 Jingwei Li,2 Gang Wang3
1Department of Neurology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou City, Liaoning Province 121001, People’s Republic of China; 2Department of Neurology, Liaoning Health Industry Group Fuxin Mine General Hospital, Jinzhou City, Liaoning Province 121001, People’s Republic of China; 3Department of Interventional Radiology, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou City, Liaoning Province 121001, People’s Republic of China
Correspondence: Gang Wang
Department of Interventional Radiology, The First Affiliated Hospital of Jinzhou Medical University, No. 2 Renmin Street, Jinzhou City, Liaoning Province 121001, People’s Republic of China
Tel +86 416 419 7026
Purpose: Galuteolin is a substance extracted and purified from honeysuckle. The purpose of this study was to explore the protective effect of galuteolin on cerebral ischemia-reperfusion injury (CIRI) and reveal its potential molecular mechanism from the perspectives of anti-apoptosis, anti-oxidation, and anti-inflammation.
Materials and methods: One hundred and fifty rats were randomly divided into five groups: sham group, ischemia-reperfusion (I/R) group, 50 mg/kg galuteolin group, 100 mg/kg galuteolin group, and 200 mg/kg galuteolin group. Middle cerebral artery occlusion (MCAO) was used to establish a rat CIRI model, different doses of galtenolin were intraperitoneal injected 2 hrs after ischemia, and then reperfusion was performed for 24 hrs. Neurological function and cerebral water content were determined, and cerebral infarct volume was evaluated by TTC staining. TUNEL staining was used to detect the apoptosis of nerve cells. Western Blot was used to detect the expressions of Akt, p-Akt, Sod1, Sod2, catalase, caspase-3, Bcl-2, and Bax. Lipid hydrogen peroxide (LPO) was determined by kit assay. The contents of vascular endothelial growth factor (VEGF) and pro-inflammatory cytokines IL-1β and TNF-α were determined by ELISA.
Results: The results showed that galuteolin could significantly reduce the cerebral infarction volume, neurologic score, and cerebral water content in a dose-dependent manner. In addition, galuteolin obviously reduced the apoptosis rate of nerve cells and the expression levels of caspase-3 and Bax, meanwhile up-regulated the expression levels of p-Akt and Bcl-2. Furthermore, galuteolin apparently inhibited the levels of LPO, Sod1, Sod2, and catalase in the cerebral infarction tissues. Moreover, galuteolin also significantly reduced the levels of pro-inflammatory factors IL-1β and TNF-α in the cerebral infarction tissues. Finally, Galuteolin markedly inhibited the expression of VEGF in cerebral infarction tissues.
Conclusion: Galuteolin exerts neuroprotective effects against CIRI by inhibiting apoptosis, oxidation, and inflammation.
Keywords: galuteolin, ischemia, reperfusion, apoptosis, oxidation, inflammation
This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License. By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.Download Article [PDF] View Full Text [HTML][Machine readable]