Kim Kwang-Youn, Son Jae Dong, Hwang Su-Jin, Lee Jong Kwang, Park Jae Young, Park Kwang Il, Oh Tae Woo
Korean Medicine (KM)-Application Center, Korea Institute of Oriental Medicine (KIOM), Daegu 41062, Republic of Korea.
Department of Veterinary Physiology, College of Veterinary Medicine, Gyeongsang National University, Jinju 52828, Republic of Korea.
Antioxidants (Basel). 2023 Jan 31;12(2):336. doi: 10.3390/antiox12020336.
Ulcerative colitis (UC) is an inflammatory bowel disease caused by various factors, including intestinal inflammation and barrier dysfunction. Herein, we determined the effects of fermented glutinous rice (FGR) on the expression of tight junction proteins and levels of inflammation and apoptosis in the dextran sodium sulfate (DSS)-induced acute colitis model. FGR was orally administered once per day to C57BL/6J mice with colitis induced by 5% DSS in drinking water. FGR administration recovered DSS-induced body weight loss and irregularly short colon lengths. FGR inhibited the DSS-induced decrease in FITC-dextran (FD)-4 permeability and myeloperoxidase activity. Moreover, FGR treatment repaired the reduction of zonula occluden-1 (ZO-1) and occludin expression and the increase in claudin-2 expression in colonic tissue relative to that following DSS administration. FGR treatment significantly recovered expression of cytokines, such as tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, in serum or respective mRNA expression in colonic tissue relative to that following DSS administration. FGR regulated levels of oxidative stress-related factors, such as malondialdehyde and glutathione, and the activity of catalase and superoxide dismutase in the colon tissue of the DSS-induced acute colitis mice model. Furthermore, FGR treatment inhibited apoptosis by reducing the activity of caspase-3 and the ratio of Bcl-2 associated X (Bax)/B-cell lymphoma 2 (Bcl-2). Collectively, FGR treatment protected the intestinal barrier from dysfunction and inhibited inflammation and apoptosis in DSS-induced colitis. Therefore, FGR may decrease the inflammatory response and be a candidate for treating and prevention inflammatory bowel disease by protecting the intestinal integrity.
溃疡性结肠炎(UC)是一种由多种因素引起的炎症性肠病,包括肠道炎症和屏障功能障碍。在此,我们确定了发酵糯米(FGR)对葡聚糖硫酸钠(DSS)诱导的急性结肠炎模型中紧密连接蛋白表达、炎症水平和细胞凋亡的影响。将FGR每天口服一次给予饮用含5% DSS的水诱导结肠炎的C57BL/6J小鼠。给予FGR可恢复DSS诱导的体重减轻和结肠长度不规则缩短。FGR抑制了DSS诱导的异硫氰酸荧光素-葡聚糖(FD)-4通透性降低和髓过氧化物酶活性。此外,与给予DSS后相比,FGR处理修复了结肠组织中闭合蛋白-1(ZO-1)和闭合蛋白表达的降低以及紧密连接蛋白-2表达的增加。与给予DSS后相比,FGR处理显著恢复了血清中细胞因子如肿瘤坏死因子(TNF)-α、白细胞介素(IL)-6和IL-1β的表达或结肠组织中各自的mRNA表达。FGR调节了DSS诱导的急性结肠炎小鼠模型结肠组织中氧化应激相关因子如丙二醛和谷胱甘肽的水平以及过氧化氢酶和超氧化物歧化酶的活性。此外,FGR处理通过降低半胱天冬酶-3的活性和Bcl-2相关X蛋白(Bax)/B细胞淋巴瘤2(Bcl-2)的比值来抑制细胞凋亡。总体而言,FGR处理保护肠道屏障功能,抑制DSS诱导的结肠炎中的炎症和细胞凋亡。因此,FGR可能减轻炎症反应,并且通过保护肠道完整性可能成为治疗和预防炎症性肠病的候选药物。