Baicalin may alleviate inflammatory infiltration in dextran sodium sulfate-induced chronic ulcerative colitis via inhibiting IL-33 expression
Baicalin may alleviate inflammatory infiltration in dextran sodium sulfate-induced chronic ulcerative colitis via inhibiting IL-33 expression
复制标题
黄芩苷可能通过抑制IL-33表达减轻右旋糖酐硫酸钠诱导的慢性溃疡性结肠炎的炎症浸润
DOI：
10.1016/j.lfs.2017.08.010
复制
发表时间：
2017
期刊：
影响因子：
6.1
通讯作者：
Liu Dong
中科院分区：
文献类型：
--
作者：
Zhang Cheng Liang;Zhang Si;He Wen Xi;Lu Jing Li;Xu Yan Jiao;Yang Jin Yu;Liu Dong
目的观察黄芩苷对慢性溃疡性结肠炎（UC）的治疗作用，并通过IL-33途径探讨其抗炎机制。在UC模型的第13天，小鼠分别接受黄芩苷50、100和150 mg/kg的剂量。进行疾病活动指数（DAI）评估以及HE和PAS染色。ELISA法测定血清TNF-α、IL-1β和IL-6水平。测定结肠髓过氧化物酶（MPO）活性和一氧化氮（NO）含量。免疫组化法检测IL-33和Ly 6/G的表达。Western blot检测IL-33蛋白和NF-κ B相关蛋白的含量。形态学和组织学分析显示黄芩苷对DSS诱导的小鼠UC有明显的减轻作用。此外，黄芩苷治疗显著降低了MPO和NO的水平。此外，在受损的结肠组织中，已发现炎症细胞因子如TNF-α，IL-1β和IL-6的水平升高，黄芩苷治疗可显著降低这些水平。结果表明，慢性UC小鼠结肠组织中IL-33和NF-κB p65蛋白水平升高。黄芩苷可显著抑制IL-33和NF-κB p65的表达，升高IκB-α的表达，其机制可能与抑制IL-33的表达和NF-κB的活化有关。
AimsTo investigate the therapeutic effect of baicalin treatment in chronic ulcerative colitis (UC), and explore the potential anti-inflammation mechanism(s) via IL-33 pathway.Main methodsUC model were established by giving three cycles of 5-day 2% dextran sodium sulfate (DSS) with two intervals of 14-day recovery in mice, totaling 43 days. At the 13th day of the UC modeling, mice received baicalin at doses of 50, 100, or 150 mg/kg, respectively. Disease activity index (DAI) assessment as well as HE and PAS staining were performed. Serum levels of TNF-α, IL-1β and IL-6 were determined by ELISA. Myeloperoxidase (MPO) activity and nitric oxide (NO) contents in colon were measured. The expressions of IL-33 and Ly6/G were examined by immunochemistry. And contents of IL-33 protein and NF-κB-related proteins were tested by Western blot.Key findingsMorphological and histological analyses revealed that baicalin administration had a significant effect on reducing the severity of DSS-induced UC in mice. Besides, baicalin treatment significantly reduced the levels of MPO and NO. Moreover, increased levels of inflammatory cytokines, such as TNF-α, IL-1β, and IL-6, have been identified in damaged colon tissue, which was noticeably reduced by baicalin treatment. Our data demonstrated that protein levels of IL-33 and NF-κB p65 were elevated in colon tissues of chronic UC mice. Baicalin treatment significantly suppressed levels of IL-33 and NF-κB p65, whereas levels of IκB-α were increased.SignificanceBaicalin treatment effectively alleviated DSS-induced chronic UC, and the protective mechanisms may involve inhibition of IL-33 expression and subsequent NF-κB activation.