Liu Jiuxi, Cai Jiapei, Fan Peng, Zhang Naisheng, Cao Yongguo
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, China.
Front Pharmacol. 2019 Dec 2;10:1385. doi: 10.3389/fphar.2019.01385. eCollection 2019.
Salidroside (Sal), as a major glycoside extracted from L., has exhibited its mighty anti-aging, anti-oxidant, anti-cancer, anti-inflammation, and neuroprotective effects in many diseases. Recently, it has showed its protective effect in colitis mice by activating the SIRT1/FoxOs pathway. Whereas, it is not known whether Sal has other protective mechanisms on dextran sulfate sodium (DSS)-induced colitis in mice. In this study, we investigated the protective effects and mechanisms of Sal on DSS-induced colitis in mice. The results demonstrated Sal was a competent candidate in the treatment of ulcerative colitis (UC). Sal remitted DSS-induced disease activity index (DAI), colon length shortening, and colonic pathological damage. Simultaneously, Sal alleviated excessive inflammation by reversing the IL-1β, TNF-α, and IL-10 protein levels in DSS-treated mice. Western blot analysis revealed that Sal inhibited p65 and p38 activation together with peroxisome proliferator-activated receptor (PPARγ) up-regulation. In addition, Sal skewed the imbalanced activation of nucleotide oligomerization domain-like receptor family pyrin domain containing 3 inflammasome and autophagy contributing to colitis recovery. The damaged intestinal barrier induced by DSS was also alleviated along with plasma lipopolysaccharides (LPS) reduction after Sal treatment. , Sal showed PPARγ-dependent anti-inflammatory effect in LPS-stimulated RAW264.7 cells. In summary, our results demonstrated that Sal might be an effective factor for UC treatment and its pharmacological value deserved further development.
红景天苷（Sal）作为从红景天中提取的一种主要糖苷，在许多疾病中已展现出强大的抗衰老、抗氧化、抗癌、抗炎和神经保护作用。最近，它通过激活SIRT1/FoxOs通路在结肠炎小鼠中显示出保护作用。然而，尚不清楚Sal对葡聚糖硫酸钠（DSS）诱导的小鼠结肠炎是否具有其他保护机制。在本研究中，我们调查了Sal对DSS诱导的小鼠结肠炎的保护作用及机制。结果表明Sal是治疗溃疡性结肠炎（UC）的有力候选药物。Sal缓解了DSS诱导的疾病活动指数（DAI）、结肠长度缩短和结肠病理损伤。同时，Sal通过逆转DSS处理小鼠中白细胞介素-1β（IL-1β）、肿瘤坏死因子-α（TNF-α）和白细胞介素-10（IL-10）的蛋白水平减轻了过度炎症。蛋白质印迹分析显示，Sal抑制p65和p38的激活，同时上调过氧化物酶体增殖物激活受体（PPARγ）。此外，Sal纠正了核苷酸寡聚化结构域样受体家族含pyrin结构域3炎性小体的失衡激活以及自噬，这有助于结肠炎的恢复。Sal治疗后，DSS诱导的受损肠屏障也得到缓解，同时血浆脂多糖（LPS）减少。此外，Sal在LPS刺激的RAW264.7细胞中显示出PPARγ依赖性抗炎作用。总之，我们的结果表明Sal可能是治疗UC的有效因子，其药理价值值得进一步开发。
