Sun Jie, Wang Xiao-Dong, Liu Hong, Xu Jian-Guo
Department of Anesthesiology, Nanjing University College of Medicine, Jinling Hospital, 305 East Zhongshan Road, Nanjing 210002, Jiangsu Province, China.
World J Gastroenterol. 2004 Apr 1;10(7):1028-31. doi: 10.3748/wjg.v10.i7.1028.
To investigate the protective effect of ketamine on the endotoxin-induced proinflammatory cytokines and NF-kappa B activation in the intestine.
Adult male Wistar rats were randomly divided into 6 groups: (a) normal saline control, (b) challenged with endotoxin (5 mg/kg) and treated by saline, (c) challenged with endotoxin (5 mg/kg) and treated by ketamine (0.5 mg/kg), (d) challenged with endotoxin (5 mg/kg) and treated by ketamine (5 mg/kg ), (e) challenged with endotoxin (5 mg/kg) and treated by ketamine (50 mg/kg), and (f) saline injected and treated by ketamine (50 mg/kg). After 1, 4 or 6 h, TNF-alpha and IL-6 mRNA were investigated in the tissues of the intestine (jejunum) by RT-PCR. TNF-alpha and IL-6 were measured by ELISA. We used electrophoretic mobility shift assay (EMSA) to investigate NF-kappa B activity in the intestine.
NF-kappa B activity, the expression of TNF-alpha and IL-6 were enhanced in the intestine by endotoxin. Ketamine at a dose of 0.5 mg/kg could suppress endotoxin-induced TNF-alpha mRNA and protein elevation and inhibit NF-kappa B activation in the intestine. However the least dosage of ketamine to inhibit IL-6 was 5 mg/kg in our experiment.
Ketamine can suppress endotoxin-induced production of proinflammatory cytokines such as TNF-alpha and IL-6 production in the intestine. This suppressive effect may act through inhibiting NF-kappa B.
研究氯胺酮对内毒素诱导的肠道促炎细胞因子及核因子-κB（NF-κB）激活的保护作用。
成年雄性Wistar大鼠随机分为6组：（a）生理盐水对照组；（b）给予内毒素（5 mg/kg）并予生理盐水处理；（c）给予内毒素（5 mg/kg）并予氯胺酮（0.5 mg/kg）处理；（d）给予内毒素（5 mg/kg）并予氯胺酮（5 mg/kg）处理；（e）给予内毒素（5 mg/kg）并予氯胺酮（50 mg/kg）处理；（f）注射生理盐水并予氯胺酮（50 mg/kg）处理。1、4或6小时后，采用逆转录聚合酶链反应（RT-PCR）检测肠道（空肠）组织中肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）mRNA。采用酶联免疫吸附测定（ELISA）法检测TNF-α和IL-6。采用电泳迁移率变动分析（EMSA）法检测肠道中NF-κB活性。
内毒素可增强肠道中NF-κB活性、TNF-α和IL-6的表达。0.5 mg/kg剂量的氯胺酮可抑制内毒素诱导的TNF-α mRNA和蛋白升高，并抑制肠道中NF-κB激活。然而在我们的实验中，抑制IL-6的氯胺酮最小剂量为5 mg/kg。
氯胺酮可抑制内毒素诱导的肠道促炎细胞因子如TNF-α和IL-6的产生。这种抑制作用可能通过抑制NF-κB发挥。
