Guo Feng, Lu Xiao-Wei, Xu Qiu-Ping
Affiliated Sir Run Run Shaw Hospital, School of Medicine, Zhejiang University, Hangzhou 310016, China.
Zhonghua Yi Xue Za Zhi. 2010 Jun 15;90(23):1645-7.
To investigate the mechanism of protective effect of Xingnaojing and Xuesaitong injections on cerebral ischemic reperfusion injury in rats.
The focal cerebral ischemia & reperfusion model was established by middle cerebral artery occlusion (MCAO). A total of 152 male SD rats were randomly assigned into 19 groups: sham operated group, Xingnaojing group, Xingnaojing plus Xuesaitong group and control group according to different reperfusion durations: 2, 4, 8, 24, 48, 72 h. Each group had 8 rats. Rats in Xingnaojing group received the ip injections of Xingnaojing (1 ml x 100 (-1) x d(-1)) until an onset of ischemia; Xingnaojing plus Xuesaitong group received the ip injections of Xingnaojing (1 ml x 100 g(-1) x d(-1)) and Xuesaitong (1 ml x 100 g(-1) x d(-1)) until an onset of ischemia; In the meantime, rats in control group received the same ip dose of saline. The levels of SOD and MDA were detected. The number of apoptotic neurons was detected by terminal-deoxynucleotidyl transferase medicated nick end labeling (TUNEL).
During ischemic reperfusion, the MDA content of brain homogenate increased while the SOD activity decreased (P < 0.05). Xingnaojing could significantly inhibit the increase of MDA after cerebral ischemic reperfusion (P < 0.05) and the decrease of SOD activity in rats. The changes of SOD and MDA were smaller in the Xingnaojing plus Xuesaitong group than those in the Xinnaojing group (P < 0.01). The number of apoptotic neurons in the Xingnaojing group was significantly lower than that in control group (P < 0.05). And the number of apoptotic neurons in the Xingnaojing plus Xuesaitong group was even lower than that in the Xingnaojing group(4,8 h: P < 0.05, 24, 48, 72 h: P < 0.01).
The Xingnaojing plus Xuesaitong injection has protective function after cerebral ischemic reperfusion.
探讨醒脑静注射液与血塞通注射液对大鼠脑缺血再灌注损伤的保护作用机制。
采用大脑中动脉阻塞法（MCAO）建立局灶性脑缺血再灌注模型。将152只雄性SD大鼠按再灌注时间分为19组：假手术组、醒脑静组、醒脑静加 血塞通组和对照组，每组8只，再灌注时间分别为2、4、8、24、48、72 h。醒脑静组大鼠于缺血开始时腹腔注射醒脑静（1 ml×100 g-1×d-1）；醒脑静加 血塞通组大鼠于缺血开始时腹腔注射醒脑静（1 ml×100 g-1×d-1）和血塞通（1 ml×100 g-1×d-1）；同时，对照组大鼠腹腔注射等体积生理盐水。检测超氧化物歧化酶（SOD）、丙二醛（MDA）水平，采用末端脱氧核苷酸转移酶介导的缺口末端标记法（TUNEL）检测凋亡神经元数量。
缺血再灌注期间，脑匀浆MDA含量升高，SOD活性降低（P<0.05）。醒脑静可明显抑制脑缺血再灌注后MDA含量的升高（P<0.05）及大鼠SOD活性的降低。醒脑静加 血塞通组SOD、MDA的变化较醒脑静组小（P<0.01）。醒脑静组凋亡神经元数量明显低于对照组（P<0.05），醒脑静加 血塞通组凋亡神经元数量低于醒脑静组（4、8 h：P<0.05，24、48、72 h：P<0.01）。
醒脑静加 血塞通注射液对脑缺血再灌注损伤具有保护作用。
