The roots of Nardostachys jatamansi inhibits lipopolysaccharide-induced endotoxin shock
The roots of Nardostachys jatamansi inhibits lipopolysaccharide-induced endotoxin shock
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DOI：
10.1007/s11418-010-0458-x
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发表时间：
2011-01-01
影响因子：
3.3
通讯作者：
Park, Sung-Joo
中科院分区：
文献类型：
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作者：
Bae, Gi-Sang;Seo, Sang-Wan;Park, Sung-Joo
jatamansi （NJ）已被用于炎症性疾病的治疗。然而，目前尚不清楚NJ是如何产生抗炎作用的。本研究采用脂多糖（LPS）诱导的内毒素休克实验模型，探讨NJ对内毒素休克的保护作用及其机制。在LPS刺激前或刺激后1 h分别给小鼠灌胃NJ根水提物（1、5、10 mg/kg）。NJ抑制lps诱导的内毒素休克和炎症介质的产生，如白细胞介素(IL)-1 β、IL-6、肿瘤坏死因子(TNF)- α和干扰素(IFN)- α / β。小鼠腹腔巨噬细胞被用来测定炎症介质的产生。在腹膜巨噬细胞中，NJ还抑制lps诱导的炎症介质的产生，如IL-1 β、IL-6、tnf - α和ifn - α / β。此外，NJ降低了丝裂原活化蛋白激酶（MAPKs）的激活以及干扰素调节因子(IRF)-1和IRF-7 mRNA的表达水平。此外，NJ治疗后减少了lps诱导的内毒素休克和炎症介质的产生。这些结果表明，NJ通过抑制MAPKs激活和IRF诱导，抑制IL-1 β、IL-6、tnf - α和ifn - α / β的产生，从而抑制内毒素休克。
Nardostachys jatamansi (NJ) has been used in the treatment of inflammatory diseases. However, it is not clear how NJ produces anti-inflammatory effects. In the present study, using an experimental model of lipopolysaccharide (LPS)-induced endotoxin shock, the protective effects and mechanisms of action of NJ were investigated. The water extract of roots of NJ was administrated to mice orally (1, 5, and 10 mg/kg) 1 h after or before LPS challenge. The administration of NJ inhibited LPS-induced endotoxin shock and the production of inflammatory mediators, such as interleukin (IL)-1 beta, IL-6, tumor necrosis factor (TNF)-alpha, and interferon (IFN)-alpha/beta. Murine peritoneal macrophages were used to determine the production of inflammatory mediators. In peritoneal macrophages, NJ also inhibited LPS-induced production of inflammatory mediators, such as IL-1 beta, IL-6, TNF-alpha, and IFN-alpha/beta. In addition, NJ reduced the activation of mitogen-activated protein kinases (MAPKs) and the level of expression of interferon regulatory factor (IRF)-1 and IRF-7 mRNA. Furthermore, post-treatment with NJ reduced LPS-induced endotoxin shock and the production of inflammatory mediators. These results suggest that NJ inhibits endotoxin shock by inhibiting the production of IL-1 beta, IL-6, TNF-alpha, and IFN-alpha/beta through the inhibition of MAPKs activation and IRF induction.