首页> 外文期刊>European Journal of Pharmacology: An International Journal >Ilexgenin A, a novel pentacyclic triterpenoid extracted from Aquifoliaceae shows reduction of LPS-induced peritonitis in mice
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Ilexgenin A, a novel pentacyclic triterpenoid extracted from Aquifoliaceae shows reduction of LPS-induced peritonitis in mice

机译:inlexgenin a,从Aquifoliaceae提取的新型五环素三萜类化合物显示出小鼠中LPS诱导的腹膜炎的降低

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摘要

Ilexgenin A (IA) is a novel pentacyclic triterpenoid, which extracted from leaves of Ilex hainanensis Merr. In the present study, we aim to explore anti-inflammatory activity of IA on LPS-induced peritonitis and its underlying molecular mechanism. The results determined that IA was capable of suppressing peritonitis in mice induced by intraperitoneal (i.p.) injection of lipopolysaccaride (LPS). Furthermore, the results showed that IA dramatically inhibited levels of inflammatory cells infiltration in peritoneal cavity and serum in LPS-induced mice peritonitis model. Besides, IA could dramatically inhibit levels of inflammatory cytokines (IL-1 beta, IL-6 and TNF-alpha) in peritoneal cavity in LPS-induced mice peritonitis model. In vitro study, the results showed that IA inhibited production of IL-1 beta, IL-6 and TNF-alpha at transcriptional and translational levels in RAW 264.7 cells induced by LPS. Furthermore, IA could suppress the LPS-induced activation of Akt and downstream degradation and phosphorylation of kappa B-alpha (I kappa B-alpha). Moreover, IA could significantly inhibit ERK 1/2 phosphorylation in RAW 264.7 cells induced by LPS. These results were concurrent with molecular docking which revealed ERK1/2 inhibition. These results demonstrated that IA might as an anti-inflammatory agent candidate for inflammatory disease therapy.
机译:ILEXGENIN A(IA)是一种新型五环三萜,其从ILEX Hainanensis Merr的叶子中提取。在本研究中,我们的目的是探讨IA对LPS诱导的腹膜炎及其潜在的分子机制的抗炎活性。结果确定IA能够抑制腹膜内诱导的小鼠诱导的小鼠腹膜炎(I.P.)注射脂多聚藻(LPS)。此外,结果表明,IA显着抑制了LPS诱导的小鼠腹膜炎模型中腹膜腔中的炎性细胞浸润水平。此外,IA可以显着抑制LPS诱导的小鼠腹膜炎模型中腹膜腔内的炎性细胞因子(IL-1β,IL-6和TNF-α)水平。在体外研究中,结果表明,IA在LPS诱导的原始264.7细胞中的转录和平移水平上抑制IL-1β,IL-6和TNF-α的产生。此外,IA可以抑制LPS诱导的AKT和下游降解和κB-α(IκB-α)的磷酸化。此外,IA可以显着抑制LPS诱导的原始264.7细胞中的ERK 1/2磷酸化。这些结果与分子对接同时显示,其显示ERK1 / 2抑制。这些结果表明,IA可以作为炎症疾病治疗的抗炎剂候选者。

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