地塞米松,噻庚啶,山莨菪碱和地诺前列酮对内毒素休克TNFα产？…

目的：研究地塞米松（Ｄｅｘ）噻庚啶（Ｃｙｐ），山莨菪碱（Ａｎｉ）和地诺前列腺酮（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ＴＮＦ，产生的抗体休克作用。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

Effects of dexamethasone, cyproheptadine, anisodamine, and dinoprostone on TNF alpha production in endotoxic shock.

AIM: To study the effects of dexamethasone (Dex), cyproheptadine (Cyp), anisodamine (Ani), and dinoprostone (Din) on lipopolysaccharides (LPS)-induced tumor necrosis factor alpha (TNF alpha) gene expression and antishock effects of inhibiting TNF alpha production. METHODS: Endotoxic shock in rats was produced by i.v. injection of LPS (E coli O111B4, 5 mg.kg-1). TNF alpha mRNA accumulation was assessed by Northern blot. Plasma TNF alpha contents were determined by radioimmunoassay. RESULTS: The TNF alpha mRNA levels in rat liver at 2 h after LPS challenge was increased obviously (autoradiograms analyzed by scanning were 38 +/- 10 vs saline control 11 +/- 8, P < 0.01). The plasma TNF alpha contents were markedly increased [(22 +/- 3) micrograms.L-1 vs saline control (2.2 +/- 1.0) micrograms.L-1, P < 0.01]. Dex 5, Cyp 5, Ani 10, or Din 2 mg.kg-1 immediately injected after i.v. LPS markedly decreased the TNF alpha mRNA levels in rat liver and plasma TNF alpha contents. The Dex, Cyp, Ani, and Din improved the mouse survival rate 24 h after LPS 20 mg.kg-1 challenge. CONCLUSION: Dex, Cyp, Ani, and Din strongly inhibit LPS-induced TNF alpha gene expression, and have a beneficial antishock effects.