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Stigmasterol Exerts Neuro-Protective Effect Against Ischemic/Reperfusion Injury Through Reduction Of Oxidative Stress And Inactivation Of Autophagy

Authors Sun J, Li X, Liu J, Pan X, Zhao Q

Received 20 June 2019

Accepted for publication 9 September 2019

Published 18 October 2019 Volume 2019:15 Pages 2991—3001

DOI https://doi.org/10.2147/NDT.S220224

Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 2

Editor who approved publication: Dr Yuping Ning


Jiadong Sun, Xuemei Li, Junling Liu, Xin Pan, Qianqian Zhao

Department of Neurology, Affiliated Hospital of Weifang Medical University, Weifang City, Shandong Province 262100, People’s Republic of China

Correspondence: Jiadong Sun
Department of Neurology, Affiliated Hospital of Weifang Medical University, No. 2428 Yuhe Road, Weifang City, Shandong Province 262100, People’s Republic of China
Tel +86 536 3081268
Email wsmztrusnx5@163.com

Purpose: Stroke remains the primary cause of pain, suffering, and death in patients. One of the major thrusts in stroke therapy is to find an effective prevention strategy. Objectives of this study are to testify the neuro-protection effect of stigmasterol in ischemic/reperfusion injury model.
Methods: The dosage-dependent effects (20, 40, and 80 mg/kg) of stigmasterol on physiological behaviors and oxidative stress biomarkers were investigated. Expression and phosphorylation of beclin1, microtubule-associated protein 1 light chain 3 (LC3), adenosine monophosphate-activated protein kinase (AMPK), mTOR, and N-terminal kinase (JNK) were detected.
Results: The results showed that stigmasterol was able to effectively reduce neurological deficits and infarct damage induced by the ischemic/reperfusion injury, improve histopathology changes, and restore the levels of the endogenous antioxidant defense system in a dose–response mode. Stigmasterol effectively depressed the expression level of beclin1, and the conversion of LC3 I to LC3 II, while promoted the phosphorylation of mTOR, and remarkably inhibited the phosphorylation of AMPK and JNK, as well as the expression of JNK induced by 24 hrs of reperfusion.
Conclusion: These findings reveal that stigmasterol has neuro-protective effect against the ischemic/reperfusion injury, possibly associated with reduction of oxidative stress and inactivation of autophagy via AMPK/mTOR and JNK pathways.

Keywords: stigmasterol, ischemia/reperfusion injury, oxidative stress, autophagy, AMPK pathway, mTOR pathway, JNK pathway
 

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