藤黄酸治疗溃疡性结肠炎的作用机制研究  

Study on the Mechanism of Luteic Acid in the Treatment of Ulcerative Colitis

作　　者：杨建荣[1] 王晓龙 陈亮 林波[1] 曹洪涛 Yang Jianrong;Wang Xiaolong;Chen Liang;Lin Bo;Cao Hongtao(Department of Gastrointestinal Surgery,Guangzhou Huadu District People's Hospital,Guangzhou 510800,Guangdong Province,China)

机构地区：[1]广州市花都区人民医院胃肠外科,广东广州510800

出　　处：《中外医药研究》2024年第26期3-5,共3页JOURNAL OF CHINESE AND FOREIGN MEDICINE AND PHARMACY RESEARCH

基　　金：广州市花都区科技计划项目(编号:22-HDWS-027)。

摘　　要：目的:研究藤黄酸治疗溃疡性结肠炎(UC)的作用机制。方法:选取SD大鼠80只,随机分为空白组(n=20)、模型组(n=20)、柳氮磺吡啶组(n=20)和藤黄酸组(n=20)。除空白组外,其余3组建立右旋糖酐硫酸钠(DSS)诱导UC大鼠模型。柳氮磺吡啶组给予柳氮磺吡啶灌胃,藤黄酸组给予藤黄酸灌胃。比较各组体质量,结肠长度,检测肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)水平,通过结肠组织病理检测p-信号转导和转录激活因子-3(STAT3)/STAT3水平。结果:给药第1天,四组体质量比较,差异无统计学意义(P>0.05);给药第5天,模型组体质量低于其他三组(P<0.05);给药第10天,模型组体质量低于其他三组,柳氮磺吡啶组与藤黄酸组低于空白组(P<0.05)。模型组结肠短于其他3组(P<0.05)。模型组TNF-α、IL-1β、IL-6水平高于其他3组(P<0.05);柳氮磺吡啶组与藤黄酸组TNF-α、IL-6水平高于空白组(P<0.05);免疫组织化学染色显示,模型组P-STAT3/STAT3高于其他3组(P<0.05)。结论:藤黄酸可以改善溃疡性结肠炎大鼠体质量、结肠长度、炎性因子水平,其机制与IL-6/STAT3信号通路有关。Objective:To study the mechanism of luteic acid in the treatment of ulcerative colitis(UC).Methods:A total of eighty SD rats were randomly divided into blank group(n=20),model group(n=20),salazopyridine group(n=20)and luteic acid group(n=20).Except the blank group,the other 3 groups established the UC rat model induced by sodium dextran sulfate(DSS).Salazopyridine group was given salazopyridine group and luteic acid group was given luteic acid group.The body weight and colon length of all groups were compared,and the levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β)and interleukin-6(IL-6)were detected.P-signal transduction and transcriptional activator 3(STAT3)/STAT3 levels were detected by colon histopathology.Results:On the first day of administration,there was no significant difference in body mass among the four groups(P>0.05);the body mass of the model group was lower than that of the other three groups on day 5 of administration(P<0.05);on the 10th day of administration,the body mass of model group was lower than that of the other three groups,and that of salazosulpyridine group and luteic acid group was lower than that of blank group(P<0.05).The colon of the model group was shorter than that of the other 3 groups(P<0.05).The levels of TNF-α,IL-1βand IL-6 in model group were higher than those in other 3 groups(P<0.05);the levels of TNF-αand IL-6 in salazopyridine group and luteic acid group were higher than those in blank group(P<0.05);immunohistochemical staining showed that P-STAT3/STAT3 in the model group was higher than that in the other three groups(P<0.05).Conclusion:Luteic acid can improve body mass,colon length and inflammatory factors in ulcerative colitis rats,and the mechanism is related to IL-6/STAT3 signaling pathway.

关 键 词：藤黄酸 IL-6/STAT3通路 溃疡性结肠炎 

分 类 号：R285.5[医药卫生—中药学]