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

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Abstract

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.

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Acknowledgments

This work was supported by a grant from the National Natural Science Foundation of China (Nos. 81071037 and 81271395).

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Correspondence to Jian-Wen Gu.

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Yang, T., Kong, B., Gu, JW. et al. Anti-apoptotic and Anti-oxidative Roles of Quercetin After Traumatic Brain Injury. Cell Mol Neurobiol 34, 797–804 (2014). https://doi.org/10.1007/s10571-014-0070-9

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  • DOI: https://doi.org/10.1007/s10571-014-0070-9

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