Abstract：
Ulcerative colitis (UC) is characterized by a chronic and protracted course and often leads to a poor prognosis. Patients with this condition often experience postoperative complications, further complicating the management of their condition. Tetrastigma hemsleyanum polysaccharide (THP) has demonstrated considerable potential as a treatment for inflammatory bowel disease. However, its underlying mechanism in the treatment of UC remains unclear. This study systematically and comprehensively investigated the effects of THP on dextran sulfate-induced UC mice and illustrated its specific mechanism of action. The colon and spleen in UC mice were restored after THP treatment. The levels of key markers, such as secretory immunoglobulin A, β-defensin, and mucin-2 were increased, collagen deposition and epithelial cell apoptosis were decreased. Notably, THP administration led to increased levels of Ki67 and tight junction proteins in colon tissue and reduced colon tissue permeability. THP contributed to the restored balance of intestinal flora. Furthermore, THP downregulated the expressions of the proinflammatory cytokines interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-17 and promoted those of the regulatory factors forkhead box protein P3. It also exerted anti-inflammatory effects by promoting suppressor of cytokine signaling (SOCS1) expression and inhibiting the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway. Our results demonstrated that THP had an efficacy comparable to that of JAK inhibitor in treating UC. In addition, THP might play a role in UC therapy through modulation of the SOCS1/JAK2/STAT3 signaling pathway and remodeling of the intestinal mucosal barrier.
摘要：
溃疡性结肠炎（UC）的特征是慢性和延长的病程，通常导致预后不良。这种情况的患者经常会出现术后并发症，使他们的病情管理更加复杂。四角大红多糖（THP）已被证明具有治疗炎症性肠病的巨大潜力。然而,其在UC治疗中的潜在机制尚不清楚.本研究系统全面地研究了THP对硫酸葡聚糖诱导的UC小鼠的作用,并阐明了其具体的作用机制。经THP处置后UC小鼠的结肠和脾脏均恢复。关键标记的级别，如分泌性免疫球蛋白A，β-防御素,和粘蛋白-2增加，胶原沉积和上皮细胞凋亡减少。值得注意的是,THP给药导致结肠组织中Ki67和紧密连接蛋白水平升高并降低结肠组织通透性。THP有助于恢复肠道菌群平衡。此外，THP下调促炎细胞因子白细胞介素(IL)-6、肿瘤坏死因子(TNF)-α的表达,和IL-17，并促进那些调节因子叉头盒蛋白P3。它还通过促进细胞因子信号抑制因子（SOCS1）表达和抑制Janus激酶2（JAK2）/信号转导和转录激活因子3（STAT3）信号通路发挥抗炎作用。我们的结果表明，THP在治疗UC方面具有与JAK抑制剂相当的功效。此外,THP可能通过调节SOCS1/JAK2/STAT3信号通路和肠黏膜屏障的重塑在UC治疗中发挥作用。
