Yang Jie, Zhou Zhiwen, Yang Qidong, Zheng Lijun, Zeng Jin
Department of Neurology, Xiangya Hospital, Central South University, Changsha 410078, China.
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Apr;35(4):321-8. doi: 10.3969/j.issn.1672-7347.2010.04.007.
To investigate the neuroprotective mechanism of tetrahydroxystilbene glucoside (TSG), a Chinese medicine, on rats after cerebral ischemia-reperfusion.
A total of 96 Sprague-Dawley male rats were divided into 4 groups (n=24): a control group, an ischemia-reperfusion (I/R) model group, a low dose TSG [60 mg/(kg.d)]group, and a high dose TSG [120 mg/(kg.d)]group. After 6 days intragastric (ig) administration of TSG or natural saline (I/R group), reversible middle cerebral artery occlusion (MCAO) model was established by intraluminal suture technique. The rats of control group were operated on while the middle cerebral artery was not blocked. At 6 h, 24 h, 48 h, and 7 d after the reperfusion, behavior test was used to evaluate the neurological deficiency of each group. The protein expressions of nerve growth factor (NGF), growth associated protein (GAP)-43, and protein kinase A catalytic subunit (PKAc) in the cortex were measured by immunohistochemical method.
Compared with the I/R group, the neurological defect scores of the 2 TSG groups were significantly lower except at 6 h after the reperfusion. Compared with the I/R group, the protein expression of NGF, GAP-43, and PKAc after the reperfusion of the 2 TSG groups increased significantly.
The protein expression of NGF may increase when treated with TSG after cerebral ischemia-reperfusion, which activates the PKA pathway and increases the protein expression of GAP-43 that protects the neuron.
探讨中药二苯乙烯苷（TSG）对大鼠脑缺血再灌注后的神经保护机制。
将96只雄性Sprague-Dawley大鼠分为4组（n = 24）：对照组、缺血再灌注（I/R）模型组、低剂量TSG[60 mg/(kg·d)]组和高剂量TSG[120 mg/(kg·d)]组。TSG或生理盐水（I/R组）灌胃给药6天后，采用腔内缝合技术建立可逆性大脑中动脉闭塞（MCAO）模型。对照组大鼠手术时大脑中动脉不阻断。再灌注后6 h、24 h、48 h和7 d，采用行为学测试评估各组神经功能缺损情况。采用免疫组织化学方法检测皮质中神经生长因子（NGF）、生长相关蛋白（GAP）-43和蛋白激酶A催化亚基（PKAc）的蛋白表达。
与I/R组相比，除再灌注后6 h外，2个TSG组的神经功能缺损评分均显著降低。与I/R组相比，2个TSG组再灌注后NGF、GAP-43和PKAc的蛋白表达显著增加。
脑缺血再灌注后用TSG治疗可能增加NGF的蛋白表达，激活PKA通路，增加保护神经元的GAP-43的蛋白表达。
