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The potential mechanisms of c-Jun amino-terminal kinase signal transduction pathway in biopterin induction in rats with endotoxic shock
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- Author:
- No author available
- Journal Title:
- CHINESE JOURNAL OF EMERGENCY MEDICINE
- Issue:
- 12
- DOI:
- 10.3760/j.issn:1671-0282.2004.12.002
- Key Word:
- 内毒素休克;生物喋呤;一氧化氮;c-Jun氨基末端激酶;信号转导
Abstract： 目的观察c-Jun氨基末端激酶(JNK)信号通路抑制剂--curcumin对内毒素休克大鼠生物喋呤(BH4)及一氧化氮(NO)表达的影响,并探讨JNK途径在生物喋呤诱生中的信号转导机制.方法建立内毒素休克模型,60只大鼠随机分为正常对照组(n＝8)、内毒素休克组(n＝32)和curcumin拮抗组(n=20).采用逆转录多聚酶链式反应测定肝、肺、肾组织三磷酸鸟苷环水解酶I(GTP-CHI)与诱生型一氧化氮合酶 (iNOS)mRNA表达水平,分别采用反相高效液相色谱法和Griess比色法测定血浆与组织中BH4、NO水平的变化.结果与正常对照组相比,内毒素使动物肝、肺、肾组织GTP-CHI基因表达和BH4水平明显升高,至伤后24 h仍持续于较高水平;与之相应,组织iNOS基因表达和NO水平亦明显升高.curcumin处理可明显下调肝、肺、肾组织GTP-CHI mRNA表达水平,并且肝组织6～24 h时、肺组织12 h时BH4水平显著降低;各组织iNOS mRNA表达及NO水平亦显著降低.结论抑制JNK信号通路能明显抑制内毒素休克鼠多器官生物喋呤/NO系统的表达,JNK途径参与了生物喋呤诱生的信号转导过程.
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