NDLI: Ursolic Acid Ameliorates Early Brain Injury After Experimental Traumatic Brain Injury in Mice by Activating the Nrf2 Pathway

Content Provider	Springer Nature Link
Author	Ding, Hui Wang, Handong Zhu, Lin Wei, Wuting
Copyright Year	2016
Abstract	Previous studies have indicated oxidative stress and inflammatory injury as significant contributors to the secondary damage associated with traumatic brain injury (TBI). Ursolic acid (UA) has been demonstrated to exert anti-oxidative and anti-inflammatory effects on cerebral ischemia by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2) pathway. However, the effects of UA on TBI remain unclear. The aim of this study is to evaluate the potential roles of UA in the activation of the Nrf2 pathway using an experimental TBI model and the underlying mechanism. Wild-type (WT) and Nrf2$^{(−/−)}$ mice were divided into eight groups: (1) sham; (2) TBI; (3) TBI + vehicle; (4) TBI + 50 mg/kg UA; (5) TBI + 100 mg/kg UA; (6) TBI + 150 mg/kg UA; (7) TBI + Nrf2$^{(−/−)}$ + vehicle; (8) TBI + Nrf2$^{(−/−)}$ + UA. All mice underwent the TBI with the exception of the sham group. The neurologic outcomes of the mice were evaluated at 24 h after TBI, as well as the expression of Nrf2, NQO1, HO1,SOD, GPx, and MDA. Treatment of UA significantly ameliorated brain edema and the neurological insufficiencies after TBI. In addition, UA treatment markedly strengthened the nuclear translocation of Nrf2 protein and increased the expression of NQO1 and HO1. Moreover, UA significantly increased the expression of AKT, an Nrf2 upstream factor, suggesting that UA play a neuroprotective role through the activation of the Nrf2-ARE signal pathway. On the contrary, UA showed no neuroprotective effect on the Nrf2$^{(−/−)}$ mice. These data indicated that UA increases the activity of antioxidant enzymes and attenuated brain injury via Nrf2 factor.
Starting Page	337
Ending Page	346
Page Count	10
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	42
Issue Number	2
e-ISSN	15736903
Language	English
Publisher	Springer US
Publisher Date	2016-10-12
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Traumatic brain injury Nrf2 Ursolic acid Neuroprotection Neurosciences Neurochemistry Biochemistry Cell Biology Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway

Tert-butylhydroquinone Ameliorates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Mice by Enhancing Nrf2-Independent Autophagy

Ursolic acid promotes the neuroprotection by activating Nrf2 pathway after cerebral ischemia in mice

Dynamic Change of Hydrogen Sulfide After Traumatic Brain Injury and its Effect in Mice

β-Caryophyllene Attenuates Focal Cerebral Ischemia-Reperfusion Injury by Nrf2/HO-1 Pathway in Rats

Deletion of Nrf2 Exacerbates Oxidative Stress After Traumatic Brain Injury in Mice

Inhibition of c-Jun N-terminal Kinase Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Through Inhibition of a Nur77 Dependent Apoptosis Pathway

Sulforaphane Ameliorates Okadaic Acid-Induced Memory Impairment in Rats by Activating the Nrf2/HO-1 Antioxidant Pathway

The Expression Changes of Cystathionine-β-synthase in Brain Cortex After Traumatic Brain Injury

Ursolic Acid Ameliorates Early Brain Injury After Experimental Traumatic Brain Injury in Mice by Activating the Nrf2 Pathway

Similar Documents

Dl-3-n-Butylphthalide (NBP) Provides Neuroprotection in the Mice Models After Traumatic Brain Injury via Nrf2-ARE Signaling Pathway

Tert-butylhydroquinone Ameliorates Early Brain Injury After Experimental Subarachnoid Hemorrhage in Mice by Enhancing Nrf2-Independent Autophagy

Ursolic acid promotes the neuroprotection by activating Nrf2 pathway after cerebral ischemia in mice

Dynamic Change of Hydrogen Sulfide After Traumatic Brain Injury and its Effect in Mice

β-Caryophyllene Attenuates Focal Cerebral Ischemia-Reperfusion Injury by Nrf2/HO-1 Pathway in Rats

Deletion of Nrf2 Exacerbates Oxidative Stress After Traumatic Brain Injury in Mice

Inhibition of c-Jun N-terminal Kinase Ameliorates Early Brain Injury After Subarachnoid Hemorrhage Through Inhibition of a Nur77 Dependent Apoptosis Pathway

Sulforaphane Ameliorates Okadaic Acid-Induced Memory Impairment in Rats by Activating the Nrf2/HO-1 Antioxidant Pathway

The Expression Changes of Cystathionine-β-synthase in Brain Cortex After Traumatic Brain Injury

Ursolic Acid Ameliorates Early Brain Injury After Experimental Traumatic Brain Injury in Mice by Activating the Nrf2 Pathway