Chen Liping, Zhang Chunyu, Cao Jingjing, Bei Ge, Wang Xiaoyu, Miao Zhiwei
Department of Gastroenterology, Zhangjiagang TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou 215600, China.
Department of TCM Classics, Wuxi TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Wuxi 214072, China.
Evid Based Complement Alternat Med. 2022 Feb 15;2022:8780514. doi: 10.1155/2022/8780514. eCollection 2022.
Yiyi Fuzi Baijiang Decoction (YFBD), an ancient prescription developed by the ancient Chinese physician, Zhang Zhongjing, has shown remarkable effects in treating ulcerative colitis (UC). However, there are few studies on its mechanism. This study was designed to explore the potential mechanism of YFBD in treating UC. The principal ingredients of YFBD were analyzed using high-performance liquid chromatography (HPLC). Dextran sulfate sodium- (DSS-) induced mice and lipopolysaccharide- (LPS-) stimulated RAW264.7 cells were used in the study. The body weight and disease activity index (DAI) of mice were recorded and analyzed for 10 days. After sacrifice, the colonic tissues were harvested. The colon length was measured, and the histopathological changes were observed by hematoxylin and eosin staining. The levels of inflammatory cytokines in mice colons and RAW246.7 cells were determined by real-time quantitative PCR and immunofluorescence. The effects of YFBD on the TLR4-mediated PI3K/Akt and NF-B pathways were determined by western blot analysis. HPLC identified five compounds in YFBD: chlorogenic acid, caffeic acid, benzoylmesaconine, benzoyl aconitine, and quercetin. YFBD alleviated weight loss, colon shortening, and colonic histopathological lesion in mice. Meanwhile, it decreased the DAI and histological score of mice with UC. In addition, YFBD remarkably decreased the levels of interleukin- (IL-) 6, IL-1, and tumor necrosis factor (TNF)- in the colons of DSS-induced mice and LPS-stimulated RAW246.7 cells. Furthermore, the expression of key proteins in TLR4-mediated PI3K/Akt and NF-B pathways significantly decreased with YFBD treatment. In conclusion, YFBD had protective effects on mice with UC, which was in part related to its anti-inflammatory effects and downregulation of TLR4-mediated PI3K/Akt and NF-B pathways.
薏苡附子败酱汤（YFBD）是中国古代医生张仲景所创制的一首古方，在治疗溃疡性结肠炎（UC）方面显示出显著疗效。然而，关于其作用机制的研究较少。本研究旨在探讨YFBD治疗UC的潜在机制。采用高效液相色谱法（HPLC）分析YFBD的主要成分。本研究使用葡聚糖硫酸钠（DSS）诱导的小鼠和脂多糖（LPS）刺激的RAW264.7细胞。记录并分析小鼠的体重和疾病活动指数（DAI），为期10天。处死后，采集结肠组织。测量结肠长度，并用苏木精和伊红染色观察组织病理学变化。通过实时定量PCR和免疫荧光法测定小鼠结肠和RAW246.7细胞中炎性细胞因子的水平。通过蛋白质免疫印迹分析确定YFBD对Toll样受体4（TLR4）介导的磷脂酰肌醇-3激酶（PI3K）/蛋白激酶B（Akt）和核因子-κB（NF-κB）信号通路的影响。HPLC鉴定出YFBD中的五种化合物：绿原酸、咖啡酸、苯甲酰新乌头原碱、苯甲酰乌头原碱和槲皮素。YFBD减轻了小鼠的体重减轻、结肠缩短和结肠组织病理学损伤。同时，它降低了UC小鼠的DAI和组织学评分。此外，YFBD显著降低了DSS诱导的小鼠结肠和LPS刺激的RAW246.7细胞中白细胞介素（IL）-6、IL-1和肿瘤坏死因子（TNF）-的水平。此外，经YFBD处理后，TLR4介导的PI_{3}K/Akt和NF-κB信号通路中关键蛋白的表达显著降低。总之，YFBD对UC小鼠具有保护作用，这部分与其抗炎作用以及下调TLR4介导的PI_{3}K/Akt和NF-κB信号通路有关。
