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目的：探讨地诺前列酮（Ｄｉｎ）对细胞因子（ＩＬ１β，ＴＮＦα，ＩＦＮγ）及脂多糖（ＬＰＳ）诱导的原代培养大鼠肝细胞一氧化氮（ＮＯ）生成的影响，以及环腺苷一磷酸（ｃＡＭＰ）信号通路在诱导过程中的作用．方法：将吲哚美辛（Ｉｎｄ），Ｄｉｎ，弗司扣林（Ｆｏｒ）及双丁酰环鸟苷一磷酸（ｄｂｃＧＭＰ）分别加入含细胞因子ＴＮＦα，ＩＬ１β，ＩＦＮγ及ＬＰＳ的培养液中，原代培养肝细胞２４ｈ后，采用Ｇｒｉｅｓ反应法测定细胞培养上清中ＮＯ含量，放射免疫法测定细胞内ｃＡＭＰ水平．结果：Ｉｎｄ明显抑制ＬＰＳ与细胞因子刺激所致ＮＯ生成，反之，Ｄｉｎ及Ｆｏｒ促进ＮＯ生成；在同样刺激条件下，Ｄｉｎ与Ｆｏｒ使细胞内ｃＡＭＰ水平增高，而在对照组细胞未观察到上述反应．ｄｂｃＧＭＰ则无论炎性刺激存在与否均无此作用．结论：Ｄｉｎ协同细胞因子及ＬＰＳ诱导肝细胞ＮＯ生成，细胞内第二信使ｃＡＭＰ通路参与此诱导过程．
Objective: To investigate the effect of dinoprostone on the production of nitric oxide (NO) in primary cultured rat hepatocytes induced by cytokines (IL1β, TNFα, IFNγ) and lipopolysaccharide (LPS) , And cyclic adenosine monophosphate (cAMP) signaling pathway in the induction of the role. Methods: Indomethacin (Ind), Din, Forrestin (For) and bisbutyryl cyclic guanosine monophosphate (dbcGMP) were added to the culture containing cytokines TNF α, IL 1 汕, IFN γ and LPS After 24 hours of primary culture, the content of NO in cell culture supernatant was determined by Gries reaction, and the intracellular cAMP level was measured by radioimmunoassay. Results: Ind significantly inhibited the NO production induced by LPS and cytokine stimulation. On the contrary, Din and For promoted the NO production. Under the same stimulation conditions, Din and For increased the intracellular cAMP level, while no response was observed in the control cells . dbcGMP no matter whether inflammatory stimuli exist or not. Conclusion: Din synergizes with cytokines and LPS to induce NO production in hepatocytes, and cAMP pathway in second messenger is involved in this induction process.