论文部分内容阅读
目的研究丹参酮Ⅰ对内毒素脂多糖(LPS)激活后巨噬细胞高迁移率族蛋白B1(HMGB1)释放和脓毒症小鼠血清HMGB1水平的影响。方法以100μg.L-1LPS激活培养巨噬细胞株RAW264.7和小鼠腹腔巨噬细胞,然后观察3.6~18.0μmol.L-1丹参酮Ⅰ对两种巨噬细胞HMGB1释放和巨噬细胞株RAW264.7HMGB1基因表达的影响。以盲肠结扎穿孔术建立脓毒症小鼠模型,观察丹参酮Ⅰ对术后不同时间脓毒症小鼠血清HMGB1水平和存活率的影响。结果丹参酮Ⅰ明显抑制LPS激活后巨噬细胞HMGB1的释放和HMGB1mRNA的表达,降低脓毒症小鼠血清HMGB1水平并明显提高存活率。结论丹参酮Ⅰ有抑制巨噬细胞释放HMGB1和保护脓毒症小鼠作用。
Objective To investigate the effect of tanshinone Ⅰ on the release of HMGB1 from macrophages and the serum level of HMGB1 in sepsis mice after lipopolysaccharide (LPS) activation. Methods The macrophage cell line RAW264.7 and mouse peritoneal macrophages were activated by 100μg.L-1 LPS. Then the effects of 3.6 ~ 18.0μmol.L-1 tanshinone Ⅰ on HMGB1 release and macrophage cell line RAW264 .7HMGB1 gene expression. The cecal ligation and perforation was used to establish a mouse model of sepsis and observe the effect of tanshinone Ⅰ on serum HMGB1 level and survival rate of septic mice at different time points after operation. Results Tanshinone Ⅰ significantly inhibited the release of HMGB1 and the expression of HMGB1 mRNA in macrophages after LPS activation, decreased the serum HMGB1 levels and significantly improved the survival rate in septic mice. Conclusion Tanshinone Ⅰ can inhibit the release of HMGB1 from macrophages and protect mice from sepsis.