Inhibition of chikusetsusaponin IVa on inflammatory responses in RAW264.7 cell line via MAPK pathway.

Guangren Xu, Hongyu Lei, Qiaoling Yuan, Huiyu Chen, Jianming Su
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引用次数: 2

Abstract

Chikusetsusaponin IVa (CHS-IVa), a saponin from herb Panacis japonicas, possesses extensive biological activities. However, the roles and underlying mechanisms of CHS-IVa on inflammation have not been fully clarified in the setting of murine macrophages. In this study, we found that CHS-IVa effectively reduced the expression of inflammatory mediators, including interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), interleukin-1β (IL-1β), cyclooxygenase (COX-2), inducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulated murine macrophage-like RAW264.7 cells. Meanwhile, CHS-IVa could also evidently bate the contents of nitric oxide (NO) and prostaglandin E2 (PGE2) in cell culture supernatants. Furthermore, the anti-inflammatory activity of CHS-IVa may be via diminishing the phosphorylation of extracellular regulated protein kinases (ERK), p38, and c-Jun N-terminal kinase (JNK). Collectively, these findings will help to understand of the anti-inflammatory effects and mechanisms of P. japonicas deeply, and suggest a validated therapeutic use as an anti-inflammatory medication.

苦参皂苷IVa通过MAPK途径抑制RAW264.7细胞系炎症反应。
千秋皂苷IVa (CHS-IVa)是一种从日本人参中提取的具有广泛生物活性的皂苷。然而,在小鼠巨噬细胞中,CHS-IVa在炎症中的作用和潜在机制尚未完全阐明。本研究发现,在脂多糖(LPS)刺激的小鼠巨噬细胞样RAW264.7细胞中,CHS-IVa可有效降低炎症介质的表达,包括白细胞介素-6 (IL-6)、肿瘤坏死因子-α (TNF-α)、白细胞介素-10 (IL-10)、白细胞介素-1β (IL-1β)、环氧合酶(COX-2)、诱导型一氧化氮合酶(iNOS)。同时,CHS-IVa还能显著降低细胞培养上清液中一氧化氮(NO)和前列腺素E2 (PGE2)的含量。此外,CHS-IVa的抗炎活性可能是通过降低细胞外调节蛋白激酶(ERK)、p38和c-Jun n末端激酶(JNK)的磷酸化而实现的。总的来说,这些发现将有助于深入了解日本假单胞菌的抗炎作用和机制,并提出一种有效的抗炎药物治疗用途。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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