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

• Published in: Cellular and molecular neurobiology Vol. 34; no. 6; pp. 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: Journal Article
• Language: English
• Published: Boston Springer US 01.08.2014
• 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; Oxidative stress; Inflammation; Traumatic brain injury; Quercetin; Apoptosis
• ISSN: 0272-4340; 1573-6830
• DOI: 10.1007/s10571-014-0070-9

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.