摘要
目的：探讨一氧化氮（ＮＯ）在内毒素血症大鼠胰岛细胞损伤中的作用机制。方法：以２ｍｇ／ｋｇ体重ＬＰＳ腹腔注射致内毒素血症大鼠为模型，观察血清、胰腺ＮＯ含量的动态变化，用β－ＮＡＤＰＨ－ｄ组化染色检测胰岛诱生型一氧化氮合酶（ｉＮＯＳ）的表达，采用单细胞凝胶电泳技术，分析外源ＮＯ供体（硝普钠）和ＬＰＳ在体外对胰岛细胞的损伤。结果：内毒素血症大鼠血清ＮＯ水平明显增高，胰腺ＮＯ含量在注射６ｈ开始增高，１２ｈ达峰值，１ｄ后恢复至正常水平，胰岛ｉＮＯＳ表达于６ｈ开始升高，１２ｈ明显增强。体外试验显示硝普钠能明显引起胰岛细胞ＤＮＡ的损伤，而ＬＰＳ作用不明显。结论：ＮＯ在内毒素血症胰岛细胞损伤中的作用机制可能是由于ＬＰＳ在体内引起炎性细胞浸润，通过炎性或非炎性细胞促进胰岛细胞ｉＮＯＳ的表达，产生ＮＯ介导胰岛细胞ＤＮＡ直接损伤所致。
Objective: To explore the mechanism of the effects of nitric oxide (NO) on islet cells during endotoxemia in rats. Methods: After the model of endotoxemia was established in rats with intraperitoneal injection of LPS (2 mg/kg), the changes in NO levels of the serum and pancreas were dynamically observed. The expression of inducible nitric oxide (iNO) in the islet was determined with β NADPH d histochemical staining. DNA damage in islet cells by the external donor of NO (sodium nitroprusside) or LPS were assessed in vitro with single cell gel electrophoresis. Results: NO level in serum was significantly increased at the 6th h, picked at the 12th h and recovered to the normal on the 1st d in the pancreas after injection. The expression of iNOS in pancreatic islet also began to be enhanced at the 6th h and significantly enhanced at the 12th h after endotoxemia. In vitro experiment showed that sodium nitroprusside markedly damaged DNA in the islet cells but LPS did not exert the same effects. Conclusion: The mechanism of the effects of NO on islet cells during endotoxemia might be that the infiltration of the inflammatory or non inflammatory cells induced by LPS stimulates the expression of iNOS that generates the NO free radicals inducing the DNA damage of islet cells.
出处
《第三军医大学学报》
CAS
CSCD
北大核心
1999年第1期42-44,共3页
Journal of Third Military Medical University
关键词
一氧化氮
胰岛细胞
内毒素血症
大鼠
nitric oxide
endotoxin
islet cell
single cell gel electrophoresis
