Anti-apoptotic and Anti-oxidative Roles of Quercetin After Traumatic Brain Injury

Experimental studies have demonstrated significant secondary damage (including cell apoptosis, blood–brain barrier disruption, inflammatory responses, excitotoxic damage, and free radical production) after traumatic brain injury (TBI). Quercetin is a natural flavonoid found in high quantities in fru...

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Published in:Cellular and molecular neurobiology 2014-08, Vol.34 (6), p.797-804
Main Authors: Yang, Tao, Kong, Bin, Gu, Jian-Wen, Kuang, Yong-Qin, Cheng, Lin, Yang, Wen-Tao, Xia, Xun, Shu, Hai-Feng
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Apoptosis - drug effects
Biomedical and Life Sciences
Biomedicine
Brain Injuries - drug therapy
Brain Injuries - metabolism
Cell Biology
Cytokines - metabolism
Disease Models, Animal
Female
Neurobiology
Neuroprotective Agents
Neurosciences
Oxidative Stress - drug effects
Quercetin - pharmacology
Rapid Communication
Rats, Sprague-Dawley
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Summary:Experimental studies have demonstrated significant secondary damage (including cell apoptosis, blood–brain barrier disruption, inflammatory responses, excitotoxic damage, and free radical production) after traumatic brain injury (TBI). Quercetin is a natural flavonoid found in high quantities in fruits and vegetables, and may be a potential antioxidant and free radical scavenger. The purpose of this study was to determine the effects of quercetin on TBI-induced upregulation of oxidative stress, inflammation, and apoptosis in adult Sprague–Dawley rats. Animals were subjected to Feeney’s weight-drop injury, thus inducing the parietal contusion brain injury model. Quercetin was administered (30 mg/kg intraperitoneal injection) 0, 24, 48, and 72 h after TBI. Quercetin reduced cognitive deficits, the number of TUNEL- and ED-1-positive cells, the protein expressions of Bax and cleaved-caspase-3 proteins, and the levels of TBARS and proinflammatory cytokines, and increased the activity of antioxidant enzymes (GSH-Px, SOD, and CAT) at 1 week after TBI. Our results suggest that in TBI rats, quercetin improves cognitive function owing to its neuroprotective action via the inhibition of oxidative stress, leading to a reduced inflammatory response, thereby reducing neuronal death.
ISSN:0272-4340
1573-6830
1573-6830
DOI:10.1007/s10571-014-0070-9