IL-23/STAT3/Th17轴在重症急性胰腺炎中的作用机制及清解化攻方的干预作用  

Mechanism of IL-23/STAT3/Th17 axis in severe acute pancreatitis and intervention effect of Qingjie Huagong decoction

作　　者：冯敏超 罗芳[1,2] 秦百君 唐曦平 李凯 陈国忠[1] FENG Minchao;LUO Fang;QIN Baijun;TANG Xiping;LI Kai;CHEN Guozhong(The First Affiliated Hospital of Guangxi University of Traditional Chinese Medicine,Nanning 530001,China;Guangxi Key Laboratory of Molecular Biology of Traditional Chinese Medicine and Preventive Medicine,Nanning 530001,China;Chongqing Hospital of Traditional Chinese Medicine,Chongqing 400011,China;Affiliated Cancer Hospital of Guangxi Medical University,Nanning 530001,China)

机构地区：[1]广西中医药大学第一附属医院,南宁530001 [2]广西中医药防治医学分子生物重点实验室,南宁530001 [3]重庆市中医院,重庆400011 [4]广西医科大学附属肿瘤医院,南宁530001

出　　处：《中国免疫学杂志》2025年第4期792-797,802,共7页Chinese Journal of Immunology

基　　金：国家自然科学基金项目(82160890);广西壮族自治区医疗卫生适宜技术开发与推广应用项目(S2019021);广西自然科学基金面上项目(2020GXNSFAA297062);广西中医药大学研究生教育创新计划项目(YCSW2023383)。

摘　　要：目的:研究IL-23/STAT3/Th17轴在重症急性胰腺炎(SAP)中的作用机制及清解化攻方的干预作用。方法:逆胰胆管注射牛磺胆酸钠建立SAP大鼠模型,分别设置空白组、模型组、不同剂量清解化攻方给药组和阳性对照组,HE染色观察胰腺组织病理,ELISA检测血清脂肪酶、α-淀粉酶、炎症指标,结合RT-qPCR、IHC、Western blot和IF技术,阐明清解化攻方保护SAP大鼠胰腺组织的作用机制。结果:清解化攻方各剂量组SAP模型大鼠血清中α-淀粉酶、脂肪酶、IL-1β、IL-6、IL-17、IL-23、TNF-α、TGF-β的含量均显著降低,且中剂量组效果最优(P<0.05);IHC和RT-qPCR结果显示,清解化攻方中、高剂量组SAP大鼠模型胰腺组织中IL-23、STAT3、IL-17蛋白和mRNA的表达量显著降低(P<0.05);另外,Western blot结果表明,清解化攻方中剂量组SAP大鼠IL-23、STAT3、p-STAT3、IL-17蛋白的表达水平明显降低(P<0.05);IF检测显示,清解化攻方各剂量均能抑制SAP大鼠Th17细胞的分化,其中中剂量抑制效果最显著(P<0.05)。结论:清解化攻方通过调控IL-23/STAT3信号通路的活化,从而抑制Th17细胞分化,发挥保护胰腺组织的作用。Objective:To investigate the mechanism of IL-23/STAT3/Th17 axis in severe acute pancreatitis(SAP)and the interventional effect of the Qingjie Huagong decoction(QJHGD).Methods:A rat model of SAP was established by injecting sodium taurocholate into the retrograde pancreatic duct.The blank group,model group,different doses of QJHGD administration groups and positive group were set up respectively.HE staining was used to observe the pathology of pancreatic tissue.ELISA was used to detect serum lipase,α-amylase and inflammatory markers.By combining RT-qPCR,IHC,Western blot,and IF techniques,we elucidated the mechanism of QJHGD in protecting pancreatic tissue in SAP rats.Results:The levels of amylase,lipase,IL-1β,IL-6,IL-17,IL-23,TNF-αand TGF-βin the serum of SAP model rats in all dose groups of QJHGD were significantly reduced,and the effect was the best in medium dose group(P<0.05).The results of IHC and RT-qPCR revealed that the medium-and high-dose groups of QJHGD significantly reduced the expression of IL-23,STAT3,IL-17 protein and mRNA in the pancreatic tissue of this model(P<0.05).Moreover,the Western blot results demonstrated that the expression of IL-23,STAT3,p-STAT3,and IL-17 proteins in SAP rats were significantly decreased in the medium-dose group of QJHGD(P<0.05);the IF assay indicated that Th17 cell differentiation in SAP rats GD regulates the activation of IL-23/STAT3/Th17 axis,thereby inhibiting Th17 cell differentiation and exerting a protective effect on pancreatic tissue.

关 键 词：清解化攻方 IL-23/STAT3信号通路 TH17细胞分化 重症急性胰腺炎 免疫 

分 类 号：R285.5[医药卫生—中药学]