摘要
目的探究溃结核心方对葡聚糖硫酸钠诱导的溃疡性结肠炎(UC)小鼠的保护作用和生效机制。方法将48只C57BL/6J小鼠随机分为正常组、模型组、美沙拉嗪组及溃结核心方低、中、高剂量组。各组小鼠除正常组外均自由饮用4%DSS溶液共6 d以构建急性UC小鼠模型。记录小鼠一般情况、疾病活动指数评分,HE染色法进行病理检测并评分,记录各组小鼠结肠长度、病理评分结果;采用q RT-PCR和IHC法检测各组小鼠结肠组织肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)表达;分别使用q RT-PCR实验和WB实验检测缺氧诱导因子-1α(HIF-1α)、核转录因子-κB(NF-κB)的m RNA和蛋白表达水平。结果相比正常组,模型组小鼠的体质量、结肠长度均明显降低(P<0.01);DAI评分、病理组织学评分、TNF-α、IL-1β、NF-κB、HIF-1αmRNA和蛋白表达水平有显著升高(P<0.05或P<0.01);小鼠的结肠黏膜结构遭破坏,有炎性细胞浸润;与模型组相比,溃结核心方中、高剂量组和美沙拉嗪组小鼠体质量、结肠长度有明显增加(P<0.05),DAI评分、病理组织学评分、TNF-α、IL-1βmRNA表达水平均明显降低(P<0.05或P<0.01),溃结核心方高剂量组和美沙拉嗪组小鼠NF-κB、HIF-1αmRNA和蛋白表达水平均明显降低(P<0.05或P<0.01),结肠黏膜病理损伤明显减轻。结论溃结核心方可显著改善DSS诱导的UC小鼠的结肠炎症,其作用机制与调节NF-κB/HIF-1α信号通路相关。
Objective:To investigate the protective effect and possible mechanism of Kuijie Hexin Decoction(KJHXD)on ulcerative colitis(UC)induced by dextran sulfate sodium(DSS)in mice.Methods:A total of 48 C57BL/6J mice were randomly divided into blank group,model group,mesalazine group,KJHXD low,medium and high dose groups.Except for the normal group,the remaining groups of mice were freely drunk with 4%DSS solu⁃tion for 6 days to establish an acute UC mouse model.The general condition of the mice was recorded,and the dis⁃ease activity index(DAI)score was recorded.After completion of the experiment,the pathological detection and scoring were carried out by HE staining,and the colon length and pathological score index of each group were re⁃corded.Real-time PCR and IHC were used to detect TNF-α,IL-1βlevels in the colon tissues of each group of mice.The mRNA and protein expression levels of HIF-1αand NF-κB in each group were detected by qRT-PCR and western blot.Results:Compared with the normal group,the body weight and colon length of mice in the mod⁃el group were significantly reduced(P<0.01);the DAI score,histopathological score,TNF-α,IL-1βmRNA expres⁃sion levels,NF-κB,HIF-1αmRNA and protein expression levels were significantly increased(P<0.05 or P<0.01);colonic mucosal structure was destroyed,and inflammatory cell infiltration appeared.Compared with the model group,the lengths of colon and the weights of mice were significantly increased(P<0.05),the expression levels of DAI score and histopathological score,TNF-α,IL-1βmRNA were significantly reduced(P<0.05 or P<0.01),NF-κB,HIF-1αmRNA and protein expression levels were significantly reduced in the KJHXD high-dose group and mesalazine group(P<0.05 or P<0.01),and the pathological damage of the colonic mucosa was signifi⁃cantly reduced.Conclusion:KJHXD can significantly improve the colon inflammation induced by DSS in UC mice,and its mechanism of action may be related to the regulation of NF-κB/HIF-1αsignaling pathway.
作者
黄李
彭云花
陈天
陆宏
杨巍
Huang Li;Peng Yunhua;Chen Tian;Lu Hong;Yang Wei(Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine,Shanghai 201203,China)
出处
《中国中医急症》
2023年第11期1906-1910,1931,共6页
Journal of Emergency in Traditional Chinese Medicine
基金
上海市临床重点专科2019年评审项目(shslczdzk04302)
上海市卫生健康委员会科研课题(20204Y0180)
上海中医药大学附属曙光医院“四明临床研究专项”(SGKJLL-202006)。
