摘要
将30只雄性SD大鼠（体重240-300g）随机分为3组，分别为对照组（不进行缺氧处理）、低氧组及NK—IR拮抗剂组，建立大鼠缺氧模型，NK—IR拮抗剂组腹腔注射P物质受体（NK—IR）拈抗剂（$3144）进行干预。观察各组大鼠肝组织病理学变化，检测肝功能指标及Tunnel法测肝凋亡细胞百分比，探讨P物质受体（NK—IR）拮抗剂对缺氧大鼠模型肝损伤的影响及其机制。结果显示：（1）缺氧模型的大鼠肝细胞肿胀，排列紊乱，气球样变性较多，并有点状坏死灶，损伤较NK‘IR拮抗剂组严重。（2）NK—IR拮抗剂组GGT[（6．7500士1．6691）u／3明显低于低氧组[（9．000O士1．4142）U／L）]（P〈0．05）；ALT、AST、ALP各组之间比较无明显差异（P〉0．05）。（3）NK—IR拮抗剂组肝细胞凋亡百分比[（26．6263士10．9348）％]明显低于低氧组[（44．5814士17．3245）％]（P〈0．05）。研究表明：P物质可能与缺氧性肝损伤有关，通过P物质受体（NK一1R）拮抗剂可能减轻缺氧性肝损伤。
To investigate the effect and mechanism of NK-1 Tachykinin receptor （NK-1R） antagonist on hypoxia in duced hepatic injury, we established the hypoxic rat model. 30 male SD rats （weighing 240-300g） were randomly divided into 3 groups： control group, and experimental groups including the hypoxia group and the NK-1R antagonist group. The rats of experimental groups underwent hypoxia, among them the NK-1R antagonist group were those with interference of NK-1R antagonist by intraperitoneal injection. Hepatic injury was evaluated by pathological stai- ning, hepatic function detection and hepatocellular apoptosis determination. Results showed hypoxia-induced hepatic injury in rats was established successfully. Edema, ballooning degeneration and spotty necrosis were found in livers in the experimental groups, among which the pathological injury in the hypoxia group was worse than that in the NK- 1R antagonist group. Moreover,GGT and the rate of hepatocellular apoptosis in the NK-1R antagonist group were obviously lower than that in the hypoxia group（P〈0. 05）. But no significant difference were found in ALT, AST and ALP between groups（P〉0. 05）. These data indicate that Substance P possibly participate in the process of hypoxiainduced hepatic injury, and NK-1R antagonist could reduce hypoxia-induced hepatic injury.
出处
《生物医学工程学杂志》
EI
CAS
CSCD
北大核心
2011年第5期992-996,共5页
Journal of Biomedical Engineering
关键词
P物质
NK-1R
缺氧
肝功能
肝细胞凋亡
Substance P t NK-1 tachykinin receptor antagonist
Hypoxia
Hepatic function t Hepatocellular apoptosis
