Int J Med Sci 2014; 11(3):282-290. doi:10.7150/ijms.7634
Protective Effect of Quercetin against Oxidative Stress and Brain Edema in an Experimental Rat Model of Subarachnoid Hemorrhage
1. Department of Neurosurgery, Tangdu Hospital, Fourth Military Medical University, Xi'an 710032, PR China.
2. Department of Neurosurgery, 463rd Hospital of PLA, Shenyang 110042, PR China.
3. Department of Neurosurgery, Wuhan General Hospital of Guangzhou Military Command, Wuhan 430070, PR China.
4. Department of Medical Administration, General Hospital of Shenyang Military Command, Shenyang 110016, PR China.
* These authors contributed equally to this work.
Dong Ys, Wang Jl, Feng Dy, Qin Hz, Wen H, Yin Zm, Gao Gd, Li C. Protective Effect of Quercetin against Oxidative Stress and Brain Edema in an Experimental Rat Model of Subarachnoid Hemorrhage. Int J Med Sci 2014; 11(3):282-290. doi:10.7150/ijms.7634. Available from http://www.medsci.org/v11p0282.htm
Quercetin has been demonstrated to play an important role in altering the progression of ischemic brain injuries and neurodegenerative diseases by protecting against oxidative stress. The effects of quercetin on brain damage after subarachnoid hemorrhage (SAH), however, have not been investigated. This study was designed to explore the effects of quercetin on oxidative stress and brain edema after experimental SAH using four equal groups (n = 16) of adult male Sprague-Dawley (SD) rats, including a sham group, an SAH + vehicle group, an SAH + quercetin10 group, and an SAH + quercetin50 group. The rat SAH model was induced by injection of 0.3 ml of non-heparinised arterial blood into the prechiasmatic cistern. In the SAH + quercetin10 and SAH + quercetin50 groups, doses of 10 mg/kg and 50 mg/kg quercetin, respectively, were directly administered by intraperitoneal injection at 30 min, 12 h, and 24 h after SAH induction. Cerebral tissue samples were extracted for enzymatic antioxidant determination, lipid peroxidation assay, caspase-3 activity and water content testing 48 h after SAH. Treatment with a high dose (50 mg/kg) of quercetin markedly enhanced the activities of copper/zinc superoxide dismutase (CuZn-SOD) and glutathione peroxidase (GSH-Px), and treatment with this dose significantly reduced the level of malondialdehyde (MDA). Caspase-3 and brain edema was ameliorated and neurobehavioral deficits improved in rats that received the high dose of quercetin. The findings suggest that the early administration of optimal dose of quercetin may ameliorate brain damage and provide neuroprotection in the SAH model, potentially by enhancing the activity of endogenous antioxidant enzymes and inhibiting free radical generation.
Keywords: Subarachnoid hemorrhage, Oxidative stress, Brain edema, Quercetin, Rat