Anti-apoptotic and Anti-oxidative Roles of Quercetin After Traumatic Brain Injury
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- 作者：Tao Yang (1) (2)
Bin Kong (1) (2)
Jian-Wen Gu (1)
Yong-Qin Kuang (1)
Lin Cheng (1)
Wen-Tao Yang (1)
Xun Xia (1) (2)
Hai-Feng Shu (1) - 关键词：Traumatic brain injury ; Quercetin ; Oxidative stress ; Inflammation ; Apoptosis
- 刊名：Cellular and Molecular Neurobiology
- 出版年：2014
- 出版时间：August 2014
- 年：2014
- 卷：34
- 期：6
- 页码：797-804
- 全文大小：1,759 KB
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Bin Kong (1) (2)
Jian-Wen Gu (1)
Yong-Qin Kuang (1)
Lin Cheng (1)
Wen-Tao Yang (1)
Xun Xia (1) (2)
Hai-Feng Shu (1)
1. Department of Neurosurgery, Chengdu Military General Hospital, No. 270, Rong Du Road, Chengdu, 610083, Sichuan, China
2. Third Military Medical University, Chongqing, 400038, China - ISSN：1573-6830
文摘
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.