Yeh Chia-Chou, Lin Chih-Che, Wang Shulhn-Der, Hung Che-Ming, Yeh Ming-Hsien, Liu Ching-Ju, Kao Shung-Te
Institute of Chinese Medical Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan.
J Ethnopharmacol. 2007 May 4;111(2):418-26. doi: 10.1016/j.jep.2006.12.014. Epub 2006 Dec 20.
To investigate the effects of Gingyo-san (GGS), the traditional Chinese medicinal formula, on the acute lung inflammation induced by LPS in vivo, mice were challenged with intratracheal LPS before treatment with GGS or vehicle. In lung morphology, GGS reduced the infiltration of activated polymorphonuclear neutrophils in the airways, decreased pulmonary edema, reduced nitrosative stress, and improved lung morphology. ELISA or RT-PCR detected the expression of cytokines in BALF and lung tissue. The mechanism of these benefits by treatment with GGS including attenuating expression TNFalpha, IL-1 beta, IL-6, KC, MCP-1, MIP-2, iNOS, and activation of nuclear factor (NF-kappaB and AP-1) in BALF and lung tissue. Particularly, GGS also enhanced the anti-inflammatory cytokine (IL-10) and limited the acute lung inflammation. Therefore, its protection activity against LPS-induced lung inflammatory mediators release might be beneficial in the treatment of endotoxin-associated inflammation.
为了研究中药方剂银杏散（GGS）对体内脂多糖（LPS）诱导的急性肺部炎症的影响，在用GGS或赋形剂处理之前，对小鼠进行气管内LPS攻击。在肺形态学方面，GGS减少了气道中活化的多形核中性粒细胞浸润，减轻了肺水肿，降低了亚硝化应激，并改善了肺形态。酶联免疫吸附测定（ELISA）或逆转录-聚合酶链反应（RT-PCR）检测支气管肺泡灌洗液（BALF）和肺组织中细胞因子的表达。GGS治疗带来这些益处的机制包括减弱BALF和肺组织中肿瘤坏死因子α（TNFα）、白细胞介素-1β（IL-1β）、白细胞介素-6（IL-6）、角质形成细胞趋化因子（KC）、单核细胞趋化蛋白-1（MCP-1）、巨噬细胞炎性蛋白-2（MIP-2）、诱导型一氧化氮合酶（iNOS）的表达以及核因子（核因子κB和活化蛋白-1）的激活。特别地，GGS还增强了抗炎细胞因子（IL-10）并限制了急性肺部炎症。因此，其对LPS诱导的肺部炎症介质释放的保护活性可能有益于内毒素相关炎症的治疗。
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