Department of Neurology, Nanjing Drum Tower Hospital Clinical College of Traditional Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing 210008, PR China.
Brain Res. 2012 Apr 4;1447:20-7. doi: 10.1016/j.brainres.2012.02.011. Epub 2012 Feb 10.
The present study investigated the neuroprotective potential of Diammonium Glycyrrhizinate (DG) in focal cerebral ischemic-reperfusion (IR) injury in mice. The middle cerebral artery occlusion (MCAO) model of the mouse was used. Mice were treated with DG (20mg/kg per day, intraperitoneal injection) or saline as control, from the beginning of the reperfusion to 7 days. The focal cerebral IR injury resulted in significant neurological deficits, infarct size, and brain water content (BWC) at 1 day, 3 days and 7 days after MCAO. A significant increase in various inflammatory mediators like interleukin-1 (IL-1), tumor necrosis factor-α (TNF-α), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NF-κB) and astrocytic glial fibrillary acidic protein (GFAP) was also observed in the IR challenged brains. The DG treatment significantly improved neurofunction, decreased infarct size, and suppressed edema in the focal cerebral IR injury. The neuroprotective effect of DG was found to be associated with significant reduction in the IL-1, TNF-α, COX-2, iNOS, NF-κB and GFAP levels. In summary, this study suggested that DG has a neuroprotective effect on cerebral IR injury and this effect is likely related to DG's anti-inflammatory function.
本研究探讨了甘草酸二铵（DG）在小鼠局灶性脑缺血再灌注（IR）损伤中的神经保护潜力。采用小鼠大脑中动脉闭塞（MCAO）模型。小鼠从再灌注开始至 7 天每天接受 DG（20mg/kg，腹腔注射）或生理盐水作为对照治疗。MCAO 后 1 天、3 天和 7 天，局灶性脑 IR 损伤导致明显的神经功能缺损、梗死面积和脑水含量（BWC）增加。IR 挑战的大脑中还观察到各种炎症介质如白细胞介素-1（IL-1）、肿瘤坏死因子-α（TNF-α）、环氧化酶-2（COX-2）、诱导型一氧化氮合酶（iNOS）和核因子-κB（NF-κB）以及星形胶质细胞纤维酸性蛋白（GFAP）的显著增加。DG 治疗显著改善了神经功能，减少了梗死面积，并抑制了局灶性脑 IR 损伤中的水肿。DG 的神经保护作用与 IL-1、TNF-α、COX-2、iNOS、NF-κB 和 GFAP 水平的显著降低有关。总之，这项研究表明 DG 对脑 IR 损伤具有神经保护作用，这种作用可能与 DG 的抗炎功能有关。
