Ginsenosides have a variety of pharmacological activities, including immunomodulatory, antitumor and anti-inflammatory activities. However, the effect of Rk3 on ulcerative colitis has rarely been reported. This study evaluated the effect of Rk3 on DSS-induced ulcerative colitis and preliminarily explored the anti-inflammatory mechanisms. Rk3 administration significantly attenuated the weight loss, increased DAI scores, colonic shortening, and increased MPO and iNOS activities caused by DSS in mice. Histological improvement was apparent, tight junctions in the colon were restored, and the levels of short-chain fatty acids (acetic acid, butyric acid and isovaleric acid) were increased. In addition, Rk3 reduced the expression of proinflammatory factors (TNF-α, IL-1β and IL-6), NLRP3, ASC, and Caspase-1, indicating blockade of the NLRP3 inflammasome pathway. These results show that Rk3 can improve DSS-induced ulcerative colitis by protecting intestinal barrier function and inhibiting NLRP3 inflammasome expression, indicating that Rk3 could be used as a potential drug for treating ulcerative colitis.

译文

人参皂苷具有多种药理活性,包括免疫调节,抗肿瘤和抗炎活性。然而,Rk3对溃疡性结肠炎的作用很少报道。本研究评估了Rk3对DSS诱导的溃疡性结肠炎的作用,并初步探讨了其抗炎机制。Rk3给药可显着减轻小鼠的体重减轻,DAI评分增加,结肠缩短以及DSS引起的MPO和iNOS活性增加。组织学改善明显,结肠中的紧密连接恢复,短链脂肪酸 (乙酸,丁酸和异戊酸) 的水平增加。此外,Rk3降低了促炎因子 (TNF-α,IL-1β 和IL-6),NLRP3,ASC和Caspase-1的表达,表明NLRP3炎症小体途径被阻断。这些结果表明,Rk3可以通过保护肠屏障功能和抑制NLRP3炎症小体表达来改善DSS诱导的溃疡性结肠炎,表明Rk3可以作为治疗溃疡性结肠炎的潜在药物。

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