论文部分内容阅读
目的：研究地塞米松（Ｄｅｘ）、噻庚啶（Ｃｙｐ）、山莨菪碱（Ａｎｉ）和地诺前列酮（Ｄｉｎ）对脂多糖（ＬＰＳ）诱导的肿瘤坏死因子（ＴＮＦα）基因表达的影响和抑制ＴＮＦα产生的抗休克作用．方法：Ｗｉｓｔａｒ大鼠静脉注射ＬＰＳ（ＥｃｏｌｉＯ１１１Ｂ４，５ｍｇ·ｋｇ－１）复制内毒素休克模型．Ｎｏｒｔｈｅｒｎ印迹杂交分析肝脏ＴＮＦαｍＲＮＡ表达，放射免疫法测定血浆ＴＮＦα的含量．结果：ＬＰＳ攻击后２ｈ肝脏ＴＮＦαｍＲＮＡ表达水平显著增高（放射性自显影扫描分析３８±１０ｖｓ盐水对照组１１±８，Ｐ＜００１）；血浆ＴＮＦα水平明显升高［（２２±３）μｇ·Ｌ－１ｖｓ盐水对照组（２２±１０）μｇ·Ｌ－１，Ｐ＜００１］．静脉注射ＬＰＳ后立即静脉注射Ｄｅｘ５，Ｃｙｐ５，Ａｎｉ１０及Ｄｉｎ２ｍｇ·ｋｇ－１均能显著降低大鼠肝脏ＴＮＦαｍＲＮＡ水平和血浆ＴＮＦα含量，提高ＬＰＳ２０ｍｇ·ｋｇ－１攻击的小鼠２４ｈ的存活率．结论：Ｄｅｘ，Ｃｙｐ，Ａｎｉ和Ｄｉｎ均能显著抑制ＬＰＳ诱导的ＴＮＦα基因表达，具有较强的抗休克作用．
OBJECTIVE: To study the effects of Dex, Cyp, Ani and Din on lipopolysaccharide (LPS) -induced tumor necrosis factor (TNF) gene expression and the effects of dexamethasone Inhibit the anti-shock effect of TNFα production. Methods: LPS (EcoliO111B4, 5 mg · kg-1) was intravenously injected into Wistar rats to replicate the endotoxic shock model. The expression of TNFα mRNA in liver was analyzed by Northern blotting and the level of plasma TNFα was determined by radioimmunoassay. Results: The expression of TNFαmRNA in liver increased significantly at 2h after LPS challenge (38 ± 10vs saline control group, 11 ± 8, P <001). Plasma TNFα levels were significantly increased [(22 ± 3) μg · L -1vs saline control group (2 2 ± 1 0) μg · L-1, P <0 01]. Immediate intravenous injection of Dex5, Cyp5, Ani10 and Din2mg · kg-1 could significantly decrease the level of TNFαmRNA and the level of TNFα in the liver and increase the survival rate of mice challenged with LPS 20mg · kg-1. Conclusion: Dex, Cyp, Ani and Din can significantly inhibit LPS-induced TNFα gene expression, with strong anti-shock effect.