双环醇对脂多糖诱导巨噬细胞iNOS蛋白的表达和NF-κB活化的抑制作用

Inhibitory effect of bicyclol on iNOS expression and NF-κB activation degradation in marcrophages induced by lipopolysaccharides

目的炎症是肝炎病毒或其它因素所致的肝损伤的一个共同特征,该文目的系研究抗肝炎新药双环醇对与炎症反应相关分子的调节作用。方法以无毒性浓度双环醇预先与巨噬细胞株RAW264.7和小鼠腹腔巨噬细胞温孵1h后,加入一定量脂多糖(LPS)共同培养适当时间以诱导上述细胞的活化,培养上清中NO2-的含量和TNF-α的水平分别用Griess试剂及L929细胞株生物法测定,用Westernblot方法测定iNOS蛋白的表达和NF-κB的活化。结果双环醇在0.1～0.5mmol.L-1剂量依赖性降低1mg.L-1LPS引起的RAW264.7和小鼠腹腔巨噬细胞NO的释放以及TNF-α的分泌,双环醇0.5mmol.L-1能够明显抑制1mg.L-1LPS引起的iNOS蛋白的表达和NF-κB的活化。结论双环醇对与炎症相关的调控因子iNOS蛋白的表达和NF-

Aim Inflammation is a common characteristic of liver injury induced by hepatitis virus or other factors. The purpose of this paper was to study the modulating effect of bicyclol, a novel anti-hepatitis drug, on related inflammatory molecules. Methods Various non-cytotoxic concentrations of bicyclol were cultured with macrophage RAW264. 7 line or mouse peritoneal macrophages for 1 h, and then added adequate lipopolysaccharide （LPS） to activate macrophages. NO and TNF-α levels in the supernatant of the culture medium were determined with Griess reagent and L929 cell bioassay, respectively. The iNOS expression and NF-κB activation were detected by Western blot method. Results Pretreatment of 0. 1 -0. 5 mmol · L^-1 bicyclol significantly inhibited NO release and TNF-α secretion from RAW264. 7 cell line and mouse peritoneal macrophages induced by 1 mg · L^-1 induced iNOS expression and NF-κB activation in the cells. Conclusion Bicyclol has suppressive effect on related inflammatory molecules iNOS expression and NF-κB activation, indicating that bicyclol possesses anti-inflammatory property.