He Miao, Yu Wan-Xin, Shen Yongmei, Zhang Jing-Na, Ni Lian-Li, Li Yue, Liu Heng, Zhao Yu, Zhao Hai-Rong, Zhang Cheng-Gui
Yunnan Provincial Key Laboratory of Entomological Biopharmaceutical R&D, College of Pharmacy, Dali University, Dali, China.
Yunnan Provincial 2011 Collaborative Innovation Center for Entomoceutics, Dali, Yunnan, China.
Iran J Basic Med Sci. 2023;26(8):882-890. doi: 10.22038/IJBMS.2023.68771.14990.
Ulcerative colitis (UC) remains an enduring, idiopathic inflammatory bowel disease marked by persistent mucosal inflammation initiating from the rectum and extending in a proximal direction. An ethanol extract of L., namely Kangfuxin (KFX), has a significant historical presence in Traditional Chinese Medicine and has been broadly utilized in clinical practice for the treatment of injury. Here, we aimed to determine the effect of KFX on 2,4,6-trinitro'benzene sulfonic acid (TNBS)-induced UC in Sprague-Dawley rats.
We established the UC model by TNBS/ethanol method. Then, the rats were subject to KFX (50, 100, 200 mg/kg/day) for 2 weeks by intragastric gavage. The body weight, disease activity index (DAI), colonic mucosal injury index (CMDI), and histopathological score were evaluated. The colonic tissue interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), IL-10, transforming growth factor-1 (TGF-β1), and epidermal growth factor (EGF) were determined by Elisa. To study T-lymphocyte subsets, flow cytometry was performed. In addition, the expression level of NF-κB p65 was evaluated by immunohistochemistry and western blot analysis.
Compared with the TNBS-triggered colitis rats, the treatment of rats with KFX significantly increased the body weight, and decreased DAI, CMDI, and histopathological score. Also, KFX elicited a reduction in the secretion of colonic pro-inflammatory cytokines, namely IL-1β, IL-6, and TNF-α, concomitant with up-regulation of IL-10, TGF-β1, and EGF levels. Upon KFX treatment, the CD3+CD4+/CD3+CD8+ ratio in the spleen decreased, while the CD3+CD8+ subset and the CD3+CD4+CD25+/CD3+CD4+ ratio demonstrated an increase. In addition, the expression of NF-κB p65 in the colon was decreased.
KFX effectively suppresses TNBS-induced colitis by inhibiting the activation of NF-κB p65 and regulating the ratio of CD4+/CD8+.
溃疡性结肠炎（UC）仍然是一种持久的特发性炎症性肠病，其特征是从直肠开始并向近端延伸的持续性粘膜炎症。L.的乙醇提取物，即康复新（KFX），在传统中医中有着重要的历史地位，并已广泛应用于临床治疗损伤。在此，我们旨在确定KFX对2,4,6-三硝基苯磺酸（TNBS）诱导的Sprague-Dawley大鼠UC的影响。
我们通过TNBS/乙醇法建立UC模型。然后，通过灌胃给予大鼠KFX（50、100、200mg/kg/天），持续2周。评估体重、疾病活动指数（DAI）、结肠粘膜损伤指数（CMDI）和组织病理学评分。通过酶联免疫吸附测定（ELISA）法测定结肠组织白细胞介素（IL）-1β、IL-6、肿瘤坏死因子-α（TNF-α）、IL-10、转化生长因子-1（TGF-β1）和表皮生长因子（EGF）。为研究T淋巴细胞亚群，进行流式细胞术检测。此外，通过免疫组织化学和蛋白质印迹分析评估NF-κB p65的表达水平。
与TNBS诱导的结肠炎大鼠相比，用KFX治疗大鼠显著增加了体重，并降低了DAI、CMDI和组织病理学评分。此外，KFX使结肠促炎细胞因子IL-1β、IL-6和TNF-α的分泌减少，同时IL-10、TGF-β1和EGF水平上调。经KFX治疗后，脾脏中CD3 + CD4 + / CD3 + CD8 + 比值降低，而CD3 + CD8 + 亚群和CD3 + CD4 + CD25 + / CD3 + CD4 + 比值升高。此外，结肠中NF-κB p65的表达降低。
KFX通过抑制NF-κB p65的激活和调节CD4 + / CD8 + 比值有效抑制TNBS诱导的结肠炎。
