NDLI: Carnosol protects against spinal cord injury through Nrf-2 upregulation.

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Carnosol protects against spinal cord injury through Nrf-2 upregulation.

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Carnosol protects against spinal cord injury through Nrf-2 upregulation.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Zhi-Hui Xie, Yu-Xi Zhang, Jun-Wei Qiu, Xiao-Hua Cheng, Ai-Bin Tian, Li Ma, Bao-Yin Hou, Yu-Bo
Description	Author Affiliation: Wang ZH ( a Department of Orthopedics , The Hospital of Yu Tian , Tangshan , P.R. China and.); Xie YX ( b Department of Intensive Care Unit , Hebei United University Affiliated Hospital , Tangshan , P.R. China.); Zhang JW ( b Department of Intensive Care Unit , Hebei United University Affiliated Hospital , Tangshan , P.R. China.); Qiu XH ( a Department of Orthopedics , The Hospital of Yu Tian , Tangshan , P.R. China and.); Cheng AB ( b Department of Intensive Care Unit , Hebei United University Affiliated Hospital , Tangshan , P.R. China.); Tian L ( a Department of Orthopedics , The Hospital of Yu Tian , Tangshan , P.R. China and.); Ma BY ( a Department of Orthopedics , The Hospital of Yu Tian , Tangshan , P.R. China and.); Hou YB ( a Department of Orthopedics , The Hospital of Yu Tian , Tangshan , P.R. China and.)
Abstract	BACKGROUND: Carnosol is an ortho-diphenolic diterpene with excellent antioxidant potential. The present study was designed to identify the protective role of carnosol against spinal cord injury (SCI)-induced oxidative stress and inflammation in Wistar rats. METHODS: In the present study, oxidative stress status was determined through estimating total antioxidant capacity, total oxidant status, lipid peroxide content, protein carbonyl and sulfhydryl levels, reactive oxygen species (ROS), antioxidant status (superoxide-dismutase, catalase, glutathione, glutathione peroxidase, glutathione-S-transferase). Inflammatory effects were determined by analyzing the expression of NF-κB and COX-2 through Western blot analysis. Further, carnosol-mediated redox homeostasis was analyzed by determining p-AKT and Nrf-2 levels. RESULTS: SCI resulted in a significant increase in oxidative stress status through increased ROS generation, total oxidant levels, lipid peroxide content, protein carbonyl and sulfhydryl levels. The antioxidant status in SCI rats was significantly reduced, indicating imbalance in redox status. In addition, the expression of NF-κB and COX-2 was significantly upregulated, while p-AKT and Nrf-2 levels were downregulated in SCI rats. However, treatment with carnosol showed a significant enhancement in the antioxidant status with concomitant decline in oxidative stress parameters. Further, carnosol treatment regulated the key proteins in inflammation and redox status through significant downregulation of NF-κB and COX-2 levels and upregulation of p-AKT and Nrf-2 expression. CONCLUSION: Thus, the present study shows for the first time on the protective role of carnosol against SCI-induced oxidative stress and inflammation through modulating NF-κB, COX-2 and Nrf-2 levels in Wistar rats.
File Format	HTM / HTML
ISSN	10799893
Issue Number	1
Volume Number	36
e-ISSN	15324281
Journal	Journal of Receptors and Signal Transduction
Language	English
Publisher	Taylor & Francis
Publisher Date	2016-01-01
Publisher Place	Great Britain (UK)
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Discipline Cell Biology Discipline Physiology Discipline Biochemistry Diterpenes, Abietane Pharmacology Nf-e2-related Factor 2 Metabolism Protective Agents Spinal Cord Injuries Prevention & Control Animals Antioxidants Blotting, Western Cytokines Enzyme-linked Immunosorbent Assay Male Nf-kappa B Oxidation-reduction Oxidative Stress Drug Effects Rats Rats, Wistar Reactive Oxygen Species Pathology Up-regulation Journal Article
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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Upregulation of NF-E2-related factor-2-dependent glutathione by carnosol provokes a cytoprotective response and enhances cell survival

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Carnosol protects against spinal cord injury through Nrf-2 upregulation.