Department of Gastroenterology, Maternal and Child Health Care Hospital of Shandong Province, Jinan 251400, China.
Department of Gastroenterology, The Affiliated Hospital of Qingdao University, Qingdao City 266000, China.
Mediators Inflamm. 2020 Sep 29;2020:9419085. doi: 10.1155/2020/9419085. eCollection 2020.
Berberine (BER), a natural isoquinoline alkaloid, has been demonstrated to have appreciable anticolitis effects. Nevertheless, the protective mechanism of BER in ulcerative colitis (UC) is barely understood. The present study was aimed at exploring the therapeutic efficacy of BER on UC in experimental colitis rat model. Rats were orally administered with BER for seven days at low and high doses (25 and 50 mg/kg/day) before AcOH intracolonic instillation. BER significantly retrieved colon inflammation and mucosal damage indicated by inhibition of macroscopic score and lessened the levels of inflammatory biomarkers (IL-1, IL-6, TNF-, MPO, and PGE2). Notable downregulation of mRNA expression of p38 MAPK and increased protein expression of TGF- were achieved by BER treatment. The anti-inflammatory potential of BER was supported by the histopathological screening of colon mucosa. In addition, BER restored colonic antioxidant capacity through elevation of GSH level and antioxidant enzymatic activities (SOD, CAT, GPx, and GR) together with reductions of both MDA and NO levels. Marked downregulation of mRNA expression is accompanied by increased Nrf2 and Hmox-1 expressions in colon specimens treated by BER. Furthermore, BER exhibited noticeable antiapoptotic activities through decreasing proapoptotic proteins (Bax and caspase-3) and lessening antiapoptotic Bcl-2 protein in the colon mucosa. Based on these findings, BER may improve colitis markedly which may be mediated by its striking antioxidant, anti-inflammatory, and antiapoptotic properties.
小檗碱 (BER) 是一种天然异喹啉生物碱,已被证明具有显著的抗结肠炎作用。然而,BER 在溃疡性结肠炎 (UC) 中的保护机制尚未被充分理解。本研究旨在探讨 BER 在实验性结肠炎大鼠模型中对 UC 的治疗效果。大鼠在醋酸(AcOH)腔内灌注前,分别用低剂量(25mg/kg/天)和高剂量(50mg/kg/天)BER 灌胃 7 天。BER 显著恢复了结肠炎大鼠的结肠炎症和黏膜损伤,表现为抑制了大体评分和降低了炎症生物标志物(IL-1、IL-6、TNF-、MPO 和 PGE2)的水平。BER 处理可显著下调 p38 MAPK 的 mRNA 表达,并增加 TGF- 的蛋白表达。BER 通过升高 GSH 水平和抗氧化酶活性(SOD、CAT、GPx 和 GR),同时降低 MDA 和 NO 水平,恢复结肠抗氧化能力,支持其抗炎潜力。此外,BER 还通过降低促凋亡蛋白(Bax 和 caspase-3)和减少结肠黏膜中抗凋亡的 Bcl-2 蛋白,表现出明显的抗凋亡活性。BER 对结肠炎的改善作用可能与其显著的抗氧化、抗炎和抗凋亡特性有关。