中国医药
中國醫藥
중국의약
CHINA MEDICINE
2009年
5期
374-376
,共3页
于萌%许静宜%张毅飞%张青%张晓青%段薇
于萌%許靜宜%張毅飛%張青%張曉青%段薇
우맹%허정의%장의비%장청%장효청%단미
代谢性内毒素血症%胰腺炎性递质%胰岛素抵抗
代謝性內毒素血癥%胰腺炎性遞質%胰島素牴抗
대사성내독소혈증%이선염성체질%이도소저항
Metabolic endotoxemia%Pancreatic inflammation%Insulin resistance
目的 观察代谢性内毒素毒血症(ME)小鼠胰腺组织脂联素、白细胞介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)及其受体CCR2 mRNA的表达,探讨ME对胰腺组织炎性反应和胰岛素抵抗的影响.方法 将纯系C57BL/6J雄性小鼠编号按随机数字法分为代谢性内毒素毒血症组6只和对照组6只,代谢性内毒素毒血症组采用皮下微型泵导人微量脂多糖,建立ME动物模型,对照组则每日泵入相应体积的生理盐水.采用实时荧光定量PCR法的相对定量分析(与GAPDH对照),检测小鼠胰腺组织脂联素、IL-6、MCP-1及其受体CCR2 mRNA的表达.结果 代谢性内毒素毒血症组小鼠空腹血糖浓度降低(P0.05);小鼠体重净增值、空腹胰岛素及胰岛素抵抗指数均升高(均P<0.05);小鼠胰腺组织中IL-6、MCP-1及CCR2 mRNA的表达均增强(均P<0.05),脂联素mRNA的表达明显减低(P<0.01).结论 代谢性内毒素血症能够增强胰腺组织中促炎因子的表达,减低抗炎因子的表达,促进胰腺组织的炎症反应,降低胰岛素敏感性.
目的 觀察代謝性內毒素毒血癥(ME)小鼠胰腺組織脂聯素、白細胞介素-6(IL-6)、單覈細胞趨化蛋白-1(MCP-1)及其受體CCR2 mRNA的錶達,探討ME對胰腺組織炎性反應和胰島素牴抗的影響.方法 將純繫C57BL/6J雄性小鼠編號按隨機數字法分為代謝性內毒素毒血癥組6隻和對照組6隻,代謝性內毒素毒血癥組採用皮下微型泵導人微量脂多糖,建立ME動物模型,對照組則每日泵入相應體積的生理鹽水.採用實時熒光定量PCR法的相對定量分析(與GAPDH對照),檢測小鼠胰腺組織脂聯素、IL-6、MCP-1及其受體CCR2 mRNA的錶達.結果 代謝性內毒素毒血癥組小鼠空腹血糖濃度降低(P0.05);小鼠體重淨增值、空腹胰島素及胰島素牴抗指數均升高(均P<0.05);小鼠胰腺組織中IL-6、MCP-1及CCR2 mRNA的錶達均增彊(均P<0.05),脂聯素mRNA的錶達明顯減低(P<0.01).結論 代謝性內毒素血癥能夠增彊胰腺組織中促炎因子的錶達,減低抗炎因子的錶達,促進胰腺組織的炎癥反應,降低胰島素敏感性.
목적 관찰대사성내독소독혈증(ME)소서이선조직지련소、백세포개소-6(IL-6)、단핵세포추화단백-1(MCP-1)급기수체CCR2 mRNA적표체,탐토ME대이선조직염성반응화이도소저항적영향.방법 장순계C57BL/6J웅성소서편호안수궤수자법분위대사성내독소독혈증조6지화대조조6지,대사성내독소독혈증조채용피하미형빙도인미량지다당,건립ME동물모형,대조조칙매일빙입상응체적적생리염수.채용실시형광정량PCR법적상대정량분석(여GAPDH대조),검측소서이선조직지련소、IL-6、MCP-1급기수체CCR2 mRNA적표체.결과 대사성내독소독혈증조소서공복혈당농도강저(P0.05);소서체중정증치、공복이도소급이도소저항지수균승고(균P<0.05);소서이선조직중IL-6、MCP-1급CCR2 mRNA적표체균증강(균P<0.05),지련소mRNA적표체명현감저(P<0.01).결론 대사성내독소혈증능구증강이선조직중촉염인자적표체,감저항염인자적표체,촉진이선조직적염증반응,강저이도소민감성.
Objective To expore the feature of pancreatic inflammation induced in a murine model of endotoxemia. Methods Metabolic endotoxemia (ME) was elicited in male C57BL/6 mice following subcutaneous implantation of an osmotic minipump, through which bacterial lipopolysaccharide (LPS) was infused at a daily rate of 300 mg/kg body weight for a total of 14 days. In the end of the experiment, the fast plasma levels of glucose and insulin, the expression of a number of inflammation-related genes, as well as other selected indices were determined. Results Significantly increased levels of net increase of body weight, fast plasma glucose and insulin, and insulin resistance were found in the group of ME mice, compared with the control mice infused with normal saline. Meanwhile, the pancreatic gene expression of adiponectin, IL-6, MCP-1, and CCR2 was also found to be significantly increased in the ME mice. Conclusion Metabolic endotoxemia can induce local inflammatory response in the pancreas, which may interfere with the pancreatic insulin production.