Asiatic acid, a triterpenoid derived from Centella asiatica, has been found to exhibit multiple bioactivities. In this study, we investigated the effects of asiatic acid on lipopolysaccharide (LPS)-induced neuroinflammation and explored the mechanism of its action in BV2 microglia. We found that asiatic acid (0.1 to 100 μM) treatment significantly attenuated nitric oxide (NO) production and inhibited inducible nitric oxide synthase (iNOS) expression in a concentration-dependent manner following LPS exposure. Asiatic acid reduced LPS-induced expression and secretion of inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in BV2 cells. In addition, asiatic acid enhanced Sirt1 expression, reduced NF-κB p65 acetylation, and suppressed NF-κB activation after LPS stimulation. However, EX-527, an inhibitor of Sirt1, abolished the inhibitory effects of asiatic acid on LPS-stimulated microglia activation. These findings suggest that asiatic acid prevents LPS-induced neuroinflammation via regulating the Sirt1/NF-κB signaling pathway.

中文翻译：

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亚洲酸通过调节Sirt1 /NF-κB信号通路 抑制BV2小胶质细胞的神经炎症

亚洲酸，一种源自积雪草的三萜类化合物被发现具有多种生物活性。在这项研究中，我们研究了积雪草酸对脂多糖（LPS）诱导的神经炎症的影响，并探讨了其在BV2小胶质细胞中的作用机理。我们发现，积雪酸（0.1至100μM）处理可显着降低一氧化氮（NO）的产生，并在LPS暴露后以浓度依赖的方式抑制诱导型一氧化氮合酶（iNOS）的表达。亚洲酸降低LPS诱导的BV2细胞中炎症细胞因子的表达和分泌，包括肿瘤坏死因子-α（TNF-α），白介素-1β（IL-1β）和白介素-6（IL-6）。此外，积雪草酸可增强LPS刺激后Sirt1的表达，减少NF-κBp65的乙酰化，并抑制NF-κB的活化。但是，Sirt1的抑制剂EX-527 取消了积雪草酸对LPS刺激的小胶质细胞活化的抑制作用。这些发现表明积雪草酸可预防LPS诱导的神经炎症通过调节Sirt1 /NF-κB信号通路。