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黄葵连肠汤通过抑制NF-κB通路和自噬减轻实验性结肠炎。

Huangkui lianchang decoction attenuates experimental colitis by inhibiting the NF-κB pathway and autophagy.

作者信息

Cheng Xudong, Du Jun, Zhou Qing, Wu Bensheng, Wang Haodong, Xu Zhizhong, Zhen Shuguang, Jiang Jieyu, Wang Xiaopeng, He Zongqi

机构信息

Suzhou TCM Hospital Affiliated to Nanjing University of Chinese Medicine, Suzhou, China.

Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.

出版信息

Front Pharmacol. 2022 Aug 22;13:951558. doi: 10.3389/fphar.2022.951558. eCollection 2022.

DOI:10.3389/fphar.2022.951558
PMID:36081930
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9446438/
Abstract

Ulcerative colitis (UC) is a chronic inflammatory colorectal disease characterized by excessive mucosal immune response activation and dysfunction of autophagy in intestinal epithelial cells. Traditional herbal preparations, including the Huangkui lianchang decoction (HLD), are effective in UC clinical treatment in East Asia, but the underlying mechanism is unclear. This study evaluated the therapeutic effects and associated molecular mechanisms of HLD in UC and . A C57BL/6 UC mouse model was established using 2.5% dextran sulfate sodium. The effects of HLD on the colonic structure and inflammation in mice were evaluated using mesalazine as the control. The anti-inflammatory effects of HLD were assessed using disease activity index (DAI) scores, histological scores, enzyme-linked immunosorbent assay, immunohistochemistry, immunofluorescence, and western blotting. HLD displayed a protective effect in UC mice by reducing the DAI and colonic histological scores, as well as levels of inflammatory cytokines and NF-κB p65 in colonic tissues. NCM460 lipopolysaccharide-induced cells were administered drug serum-containing HLD (HLD-DS) to evaluate the protective effect against UC and the effect on autophagy. HLD-DS exhibited anti-inflammatory effects in NCM460 cells by reducing the levels of inflammatory cytokines and increasing interleukin 10 levels. HLD-DS reduced p-NF-κB p65, LC3II/I, and Beclin 1 expression, which suggested that HLD alleviated colitis by inhibiting the NF-κB pathway and autophagy. However, there was no crosstalk between the NF-κB pathway and autophagy. These findings confirmed that HLD was an effective herbal preparation for the treatment of UC.

摘要

溃疡性结肠炎(UC)是一种慢性炎症性结直肠疾病,其特征在于黏膜免疫反应过度激活和肠上皮细胞自噬功能障碍。包括黄葵连肠汤(HLD)在内的传统草药制剂在东亚地区的UC临床治疗中有效,但其潜在机制尚不清楚。本研究评估了HLD在UC中的治疗效果及相关分子机制。使用2.5%葡聚糖硫酸钠建立C57BL/6 UC小鼠模型。以美沙拉嗪作为对照,评估HLD对小鼠结肠结构和炎症的影响。使用疾病活动指数(DAI)评分、组织学评分、酶联免疫吸附测定、免疫组织化学、免疫荧光和蛋白质印迹法评估HLD的抗炎作用。HLD通过降低DAI和结肠组织学评分以及结肠组织中炎症细胞因子和NF-κB p65的水平,对UC小鼠发挥保护作用。将含HLD的药物血清(HLD-DS)给予脂多糖诱导的NCM460细胞,以评估其对UC的保护作用及对自噬的影响。HLD-DS通过降低炎症细胞因子水平和增加白细胞介素10水平,在NCM460细胞中发挥抗炎作用。HLD-DS降低了p-NF-κB p65、LC3II/I和Beclin 1的表达,这表明HLD通过抑制NF-κB途径和自噬减轻结肠炎。然而,NF-κB途径和自噬之间没有相互作用。这些发现证实HLD是一种治疗UC的有效草药制剂。

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