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Anti-inflammatory effects of Stephania tetrandra S. Moore on interleukin-6 production and experimental inflammatory disease models

机译:千金藤对白细胞介素6产生和实验性炎症疾病模型的抗炎作用

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摘要

Deregulation of interleukin-6 (IL-6) expression caused the synthesis and release of many inflammatory mediators. It is involved in chronic inflammation, autoimmune diseases, and malignancy. Stephania tetrandra S. Moore is a Chinese medicinal herb which has been used traditionary as a remedy for neuralgia and arthritis in China. To investigate the anti-inflammatory effects of S. tetrandra S. Moore in vitro and in vivo, its effects on the production of IL-6 and inflammatory mediators were analysed. When human monocytes/macrophages stimulated with silica were treated with 0.1–10 μg/ml S. tetranda S. Moore, the production of IL-6 was inhibited up to 50%. At these concentrations, it had no cytotoxicity effect on these cells. It also suppressed the production of IL-6 by alveolar macrophages stimulated with silica. In addition, it inhibited the release of superoxide anion and hydrogen peroxide from human monocytes/macrophages. To assess the anti-fibrosis effects of S. tetrandra S. Moore, its effects on in vivo experimental inflammatory models were evaluated. In the experimental silicosis model, IL-6 activities in the sera and in the culture supernatants of pulmonary fibroblasts were also inhibited by it. In vitro and in vivo treatment of S. tetrandra S. Moore reduced collagen production by rat lung fibroblasts and lung tissue. Also, S. tetrandra S. Moore reduced the levels of serum GOT and GPT in the rat cirrhosis model induced by CCL4, and it was effective in reducing hepatic fibrosis and nodular formation. Taken together, these data indicate that it has a potent anti-inflammatory and antifibrosis effect by reducing IL-6 production.
机译:白细胞介素6(IL-6)表达的失调引起许多炎症介质的合成和释放。它涉及慢性炎症,自身免疫性疾病和恶性肿瘤。千金藤(Stephania tetrandra S. Moore)是一种中草药,在中国传统上被用作治疗神经痛和关节炎的药物。为了研究沙门氏菌在体外和体内的抗炎作用,分析了其对IL-6和炎性介质产生的影响。当用0.1-10μg/ ml的链霉菌穆尔链霉菌处理被二氧化硅刺激的人单核细胞/巨噬细胞时,IL-6的产生被抑制高达50%。在这些浓度下,它对这些细胞没有细胞毒性作用。它还抑制了二氧化硅刺激的肺泡巨噬细胞产生IL-6的能力。另外,它抑制了人单核细胞/巨噬细胞中超氧阴离子和过氧化氢的释放。为了评估S.tetrandra S. Moore的抗纤维化作用,评估了其对体内实验性炎症模型的作用。在实验性矽肺病模型中,它也抑制了血清和肺成纤维细胞培养上清液中的IL-6活性。鼠伤寒沙门氏菌的体外和体内治疗减少了大鼠肺成纤维细胞和肺组织产生的胶原蛋白。此外,四生链霉菌S. Moore降低了由CCL4诱导的大鼠肝硬化模型中的血清GOT和GPT水平,并且对减少肝纤维化和结节形成有效。综上所述,这些数据表明它通过减少IL-6的产生具有有效的抗炎和抗纤维化作用。

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