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目的：研究噻庚啶山菪碱对内毒素休克TNFα况表达的影响。方法：Wistar臣鼠脉注射脂多糖（LPS，EcoliO111B45mg/kg)复制内毒素休克模型。Northem印迹杂交分析肝脏TNFαmRNA表达，放射免疫法测定血浆TNFαW的含量。结果：LPS攻击后2h，大鼠肝脏TNFαmRNA表达显著高于盐水对照；（杂交信号经扫描仪半定量分析对．兀19幼。盐水对照11．防止7．m，P＜001）；血浆TNFα流水平明显升高：（211.52±3.16）μg/LvsLPS攻击前（2.19±0．95）μg/L，P＜0．01。静脉注射IPs后立即给予噻庚啶（Cyp，5mg/kg）、山茛菪碱（Ami，10mg/kg），均能显著抑制LPS诱导的大鼠肝脏TNFαmRNA表达，降低血浆TNFα流含量；提高休克大鼠的平均动脉血压（MAB）及休克小鼠的24h的存活率。结论：Cyp和Ani均显著抑制内毒素休克TNFα基因表达，具有较强的抗休克作用。
OBJECTIVE: To study the effect of anisodamine on the expression of TNFα in endotoxin shock. Methods: Wistar rats were injected lipopolysaccharide (LPS, EcoliO111B45mg / kg) to replicate the endotoxic shock model. The expression of TNFαmRNA in liver was analyzed by Northern blot and radioimmunoassay. Results: The expression of TNFαmRNA in rat liver was significantly higher than that of saline control at 2h after LPS challenge (the signal of hybridization was analyzed by semiquantitative analysis by scanner. (211.52 ± 3.16) μg / L vs LPS pre-challenge (2.19 ± 0.95) μg / L, P <0.01. Immediate administration of thiophentane (Cyp, 5 mg / kg) and anisodamine (Ami, 10 mg / kg) after intravenous injection of IPs significantly inhibited LPS-induced TNFα mRNA expression in the liver and decreased the level of TNFα in plasma. Mean arterial blood pressure (MAB) in rats and survival in shock mice at 24 h. Conclusion: Both Cyp and Ani can significantly inhibit TNFα gene expression in endotoxin shock and have strong anti-shock effect.