Chronic inflammation of the myelin sheath is the crucial event behind the progression of multiple sclerosis (MS). Bacoside-A is one of the major constituents obtained from Bacopa monerii (L.) Wettst., and possess neuroprotective as well as anti-inflammatory actions. The current study explores the effect of Bacoside-A in acute and chronic models of Experimental Autoimmune Encephalomyelitis (EAE). The results indicate that the Bacoside-A treated mice produced a significant reduction in disease score compared to disease control in both models. The treatment with Bacoside-A downregulated the inflammatory cytokines (IL-6, IL-17a, and TNFα) and inflammatory chemokine CCL-5 in EAE mice. On the other hand, Bacoside-A treated mice showed a nonsignificant effect on promoting the expressions of NCAM, BDNF1, and FOXP3 in acute and chronic models of EAE. Histopathological analysis revealed that the Bacoside-A treated mice at a dose of 10 mg/kg exhibited a significant reduction in cellular infiltrations, cellular changes, and demyelination in cerebral tissues, but unable to protect at a higher dose in both models. In conclusion, Bacoside-A can able to inhibit the progression of EAE may be by the inhibition of inflammatory cytokines and chemokine evolved during active EAE.

中文翻译：

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Bacoside-A 抑制实验性自身免疫性脑脊髓炎中的炎性细胞因子和趋化因子


髓鞘的慢性炎症是多发性硬化症 （MS） 进展背后的关键事件。假马齿苋苷-A 是从假马齿苋 （L.） Wettst. 获得的主要成分之一，具有神经保护和抗炎作用。目前的研究探讨了 Bacoside-A 在实验性自身免疫性脑脊髓炎 （EAE） 的急性和慢性模型中的影响。结果表明，在两种模型中，与疾病对照相比，Bacoside-A 处理的小鼠的疾病评分显着降低。Bacoside-A 治疗下调了 EAE 小鼠的炎性细胞因子 （IL-6 、 IL-17a 和 TNFα） 和炎性趋化因子 CCL-5。另一方面，Bacoside-A 处理的小鼠在 EAE 的急性和慢性模型中对促进 NCAM 、 BDNF1 和 FOXP3 的表达没有显着影响。组织病理学分析显示，剂量为 10 mg/kg 的 Bacoside-A 处理的小鼠在脑组织中表现出细胞浸润、细胞变化和脱髓鞘的显着减少，但在两种模型中都无法在较高剂量下提供保护。总之，Bacoside-A 能够抑制 EAE 的进展可能是通过抑制活性 EAE 期间产生的炎性细胞因子和趋化因子。