[1]汪六林,李刚,刘祺,等.大黄素调节消皮素蛋白E通路的细胞焦亡改善UUO小鼠肾脏纤维化的机制研究[J].陕西中医,2026,(3):291-296.[doi:DOI:10.3969/j.issn.1000-7369.2026.03.001]
 WANG Liulin,LI Gang,LIU Qi,et al.Study on the mechanism of emodin regulating GSDME pathway-induced pyroptosis to improve renal fibrosis in UUO mice[J].,2026,(3):291-296.[doi:DOI:10.3969/j.issn.1000-7369.2026.03.001]
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大黄素调节消皮素蛋白E通路的细胞焦亡改善UUO小鼠肾脏纤维化的机制研究

《陕西中医》[ISSN:1000-7369/CN:61-1281/TN]

卷:
期数:
2026年3期
页码:
291-296
栏目:
出版日期:
2026-03-05

文章信息/Info

Title:
Study on the mechanism of emodin regulating GSDME pathway-induced pyroptosis to improve renal fibrosis in UUO mice
作者:
汪六林1234李刚1234刘祺1234王瑞1234王紫琳1234崔梦迪5金善善12345
(1.湖北省中医院,湖北 武汉 430063;2.中医肝肾研究及应用湖北省重点实验室,湖北中医药大学附属医院,湖北 武汉 430063;3.湖北时珍实验室,湖北 武汉 430063;4.湖北省中医药研究院,湖北 武汉 430063;5.湖北中医药大学,湖北 武汉 430061)
Author(s):
WANG Liulin1234LI Gang1234LIU Qi1234WANG Rui1234WANG Zilin1234CUI Mengdi5JIN Shanshan12345
(1.Hubei Provincial Hospital of Traditional Chinese Medicine,Wuhan 430063,China;2.Hubei Key Laboratory of Theory and Application Research of Liver and Kidney in Traditional Chinese Medicine,Affiliated Hospital of Hubei University of Chinese Medicine,Wuhan 430063,China;3.Hubei Shizhen Laboratory,Wuhan 430063,China;4.Hubei Province Academy of Traditional Chinese Medicine,Wuhan 430063,China;5.Hubei University of Chinese Medicine,Wuhan 430061,China)
关键词:
慢性肾脏病大黄素肾纤维化炎症因子细胞焦亡消皮素蛋白E
Keywords:
Chronic kidney diseaseEmodinRenal fibrosisInflammatory factorPyroptosisGasdermin E
分类号:
R 692.9
DOI:
DOI:10.3969/j.issn.1000-7369.2026.03.001
文献标志码:
A
摘要:
目的:探讨大黄素对慢性肾脏病(CKD)肾脏纤维化的干预作用及消皮素蛋白E(GSDME)介导的细胞焦亡的影响。方法:将雄性C57BL6小鼠按计算机生成的随机数随机分为假手术组(Sham组)、单侧输尿管梗阻模型组(UUO 组)和大黄素中药干预UUO 组(大黄素组),每组8只。干预结束后进行小鼠肾功能中血尿素氮、血肌酐和血尿酸的检测,肾组织病理损伤检测,酶联免疫吸附测定(ELISA)检测炎症因子白细胞介素(IL)-1β和IL-18,TUNEL染色观察肾组织细胞凋亡,Western blot分析肾组织细胞焦亡相关蛋白半胱氨酸天冬氨酸蛋白酶(Caspase)-3、GSDME-N 和 GSDME-FL,纤维化相关蛋白胶原蛋白(Collagen)Ⅰ、α-平滑肌肌动蛋白(SMA)的变化。结果:构建UUO模型小鼠,结果发现大黄素能有效改善小鼠肾功能,减轻肾组织病理损伤,降低炎症因子表达,减轻细胞凋亡,抑制纤维化的生成,并通过调控GSDME介导的细胞焦亡途径发挥作用。结论:大黄素可能通过调控GSDME介导的细胞焦亡途径减轻炎症因子的表达,改善肾脏纤维化。
Abstract:
Objective:To explore the intervention effect of emodin on renal fibrosis in chronic kidney disease (CKD) and its influence on gasdermin E (GSDME)-mediated pyroptosis.Methods:The male C57BL6 mice were randomly divided into the sham operation group (Sham group),the unilateral ureteral obstruction model group (UUO group),and the rhodanine-based traditional Chinese medicine intervention group for UUO (rhodanine group) according to the randomly generated numbers by the computer,with 8 mice in each group.After intervention,the renal function of mice (blood urea nitrogen,serum creatinine and blood uric acid) was detected,renal tissue pathological damage was examined,inflammatory factors (IL-1β and IL-18) were detected by ELISA,apoptosis of renal tissue cells was observed by TUNEL staining,and the changes of pyroptosis-related proteins Caspase-3,GSDME-N and GSDME-FL,fibrosis-related proteins CollagenⅠand α-SMA in renal tissue cells were analyzed by Western blot.Results:The UUO model mice were successfully constructed.It was found that emodin could effectively improve the renal function of mice,reduce renal tissue pathological damage,lower the expression of inflammatory factors,alleviate cell apoptosis,and inhibit the formation of fibrosis,and exert its effect through regulating the GSDME-mediated pyroptosis pathway.Conclusion:Emodin may alleviate the expression of inflammatory factors and improve renal fibrosis by regulating the GSDME-mediated pyroptosis pathway.

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备注/Memo

备注/Memo:
国家自然科学基金资助青年项目(82405273);湖北省自然科学基金资助青年项目(2023AFB348);湖北省自然科学基金创新发展联合基金资助重点项目(2025AFD473);湖北省自然科学基金创新发展联合基金资助培育项目(2025AFD530);湖北省自然科学基金联合基金资助项目(2024AFD300)
更新日期/Last Update: 2026-03-05