盐酸青藤碱对DSS诱导溃疡性结肠炎小鼠肠道炎症损伤的影响及其机制  

Effect and mechanism of sinomenine hydrochloride on inflammatory intestinal injury in mice with ulcerative colitis induced by DDS

作　　者：谢小荣 吕晓丹[2] 范俊华[1] 李世权 詹灵凌[2] 吕小平[1] XIE Xiaorong;LYU Xiaodan;FAN Junhua;LI Shiquan;ZHAN Lingling;LYU Xiaoping(Departement of Gastroenterology,The First Affiliated Hospital of Guangxi Medical University,Nanning 530021,China;不详)

机构地区：[1]广西医科大学第一附属医院消化内科,南宁530021 [2]广西医科大学第一附属医院检验科

出　　处：《山东医药》2023年第1期15-18,共4页Shandong Medical Journal

基　　金：国家自然科学基金资助项目(81860104);广西医疗卫生适宜技术开发与推广应用项目(S2018049);广西壮族自治区卫生健康委员会自筹经费科研课题(Z20200398);广西医科大学青年科学基金项目(GXMUYSF201913)。

摘　　要：目的探讨盐酸青藤碱(SIN)对葡聚糖硫酸钠(DSS)诱导溃疡性结肠炎小鼠肠道炎症损伤的影响及其机制。方法选择雄性C57BL/6J小鼠18只,随机分为对照组、模型组、SIN组,每组6只。模型组和SIN组予3%DSS溶液自由饮用诱导结肠炎。SIN组在建模同时予100 mg/(kg·d)SIN溶液灌胃。建模结束,评估疾病活动指数(DAI)评分,处死小鼠,剪取结肠组织,测量结肠长度,观察结肠组织病理形态学变化并评估组织学损伤评分表达。采用ELISA法检测结肠组织TNF-α、IL-6、IL-10含量,采用免疫组化法检测结肠组织自噬相关蛋白Beclin1、LC3B、p62表达。结果与对照组比较,模型组DAI评分显著升高,结肠长度显著缩短,结肠黏膜结构遭到破坏并出现明显炎症细胞浸润,组织学损伤评分显著升高,结肠组织TNF-α、IL-6含量及p62相对表达量显著升高,而IL-10含量及Beclin1、LC3B相对表达量显著降低(P均<0.05)。与模型组比较,SIN组DAI评分有所降低,结肠长度有所延长,结肠黏膜结构破坏及炎症细胞浸润有所改善,组织学损伤评分显著降低,结肠组织TNF-α、IL-6含量及p62相对表达量显著降低,而IL-10含量及Beclin1、LC3B相对表达量显著升高(P均<0.05)。结论SIN可改善DSS诱导溃疡性结肠炎小鼠肠道炎症损伤,其机制可能与SIN能够部分解除炎症所致的自噬抑制状态有关。Objective To investigate the effect of sinomenine hydrochloride(SIN)on intestinal inflammatory injury induced by dextran sodium sulfate(DSS)in ulcerative colitis mice and to explore its mechanism.Methods Eighteen male C57BL/6J mice were randomly divided into the normal control group,model group,and SIN group,with six mice in each group.Mice in the model group and SIN group were given 3%DSS free drinking to induce colitis.Mice in the SIN group were given 100 mg/(kg·d)SIN during modeling.Disease activity index(DAI)scores were evaluated at the end of modeling,and mice were killed and the length of the colon was measured,the pathological changes of the colon were observed,and the histological damage scores were evaluated.The levels of tumor necrosis factor-α(TNF-α),interleukin(IL)-6,and IL-10 in colon were detected by enzyme linked immunosorbentassay(ELISA).The expression levels of autophagy-related proteins Beclin1,LC3B and p62 in colon were detected by immunohistochemistry.Results Compared with the normal control group,DAI scores increased significantly,colon was obviously shortened,colon mucosal structure was destroyed and there were obvious inflammatory cells infiltration,histological damage scores increased,the expression levels of TNF-α,IL-6 and p62 in the colon tissues increased significantly,and the expression levels of IL-10,Beclin1 and LC3B significantly decreased in the model group(all P<0.05).Compared with model group,DAI scores decreased,colon was extended,colon mucosal structure destruction and inflammatory cells infiltration were improved and histological damage scores were significantly reduced,the TNF-α,IL-6,and p62 expression level in the colon tissues significantly decreased,while the IL-10,Beclin1 and LC3B expression levels significantly increased in the SIN group(all P<0.05).Conclusion SIN can alleviate the intestinal inflammatory damage in mice with ulcerative colitis induced by DSS,and the mechanism may be that SIN can partially relieve the inflammation-induced autophagy inhibition.

关 键 词：溃疡性结肠炎 盐酸青藤碱 自噬 小鼠 

分 类 号：R574[医药卫生—消化系统]