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粉葛水提物对2 型糖尿病db/db 小鼠胰岛细胞炎症损伤的改善作用及其机制
引用本文:朱洪杨,刘烨,容子玲,李玉婷,常诗瑶,刘玉晖. 粉葛水提物对2 型糖尿病db/db 小鼠胰岛细胞炎症损伤的改善作用及其机制[J]. 食品研究与开发, 2024, 45(1): 34-42
作者姓名:朱洪杨  刘烨  容子玲  李玉婷  常诗瑶  刘玉晖
作者单位:1. 江西中医药大学,江西南昌 330004;2. 南昌大学第二附属医院,江西南昌 330008
基金项目:国家重点研发计划项目(2017YFC1702902);江西中医药大学校级科技创新团队发展计划项目(CXTD22007)
摘    要:为探讨粉葛水提物对2型糖尿病db/db小鼠胰岛细胞炎症损伤的作用及机制,将30只db/db小鼠随机分为模型组、粉葛水提物高、中、低剂量组和二甲双胍组,正常组则采用6只db/m小鼠。持续给药8周后,测量小鼠体质量变化、计算胰重比、检测血清空腹胰岛素(fasting serum lisulin,FINS)、血清空腹血糖(fasting blood glucose,FBG)、糖化血清蛋白(glycosylated serum protein,GSP),计算胰岛素抵抗指数(homeostasis model assess-ment for insulin resistance,HOMA-IR);苏木素-伊红(hematoxylin-eosin,HE)染色观察胰腺组织病理学变化;免疫组化(immunohistochemistry,IHC)法检测胰岛细胞中肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、核因子-κBp65(nuclear factor kappa-Bp65,NF-κBp65)和白细胞介素18(interleukin-18,IL-18)的蛋白表达;蛋白...

关 键 词:粉葛水提物  2型糖尿病  胰岛细胞  炎症损伤  NLRP3炎性小体
收稿时间:2023-05-30

Ameliorating Effect and Mechanism of Puerariae thomsonii Radix Aqueous Extract on Inflammatory Damage of Islet Cells in Type 2 Diabetic db/db Mice
ZHU Hongyang,LIU Ye,RONG Ziling,LI Yuting,CHANG Shiyao,LIU Yuhui. Ameliorating Effect and Mechanism of Puerariae thomsonii Radix Aqueous Extract on Inflammatory Damage of Islet Cells in Type 2 Diabetic db/db Mice[J]. Food Research and Developent, 2024, 45(1): 34-42
Authors:ZHU Hongyang  LIU Ye  RONG Ziling  LI Yuting  CHANG Shiyao  LIU Yuhui
Affiliation:1. Jiangxi University of Chinese Medicine,Nanchang 330004,Jiangxi,China;2. The Second Affiliated Hospital of Nanchang University,Nanchang 330008,Jiangxi,China
Abstract:This paper examined the impact and mechanism of aqueous extract of Puerariae thomsonii Radix(PTR)on inflammatory damage of islet cells in type 2 diabetic db/db mice. Six db/m mice were selected as the normal group and thirty db/db mice were randomly assigned to the model group,high-,medium-,low-dose PTR aqueous extract groups,and metformin group. Eight weeks after administration,the change in body weight of the mice,the pancreas-to-weight ratio,fasting serum insulin(FINS),fasting blood glucose(FBG),glycosylated serum protein(GSP),and homeostasis model assessment for insulin resistance(HOMA-IR)were determined. Hematoxylin-eosin(HE)staining was used to observe the histopathological changes in pancreas.The protein expressions of tumor necrosis factor-α(TNF-α),nuclear factor kappa-Bp65(NF-κBp65)and interleukin - 18(IL - 18)in islet cells were detected by immunohistochemistry(IHC). Western blot was conducted to identify the expressions of NOD-like receptor thermoprotein domain 3(NLRP3),apoptosis-associated speck-like protein containing a caspase recruitment domain(ASC),cystein-asparate protease 1(caspase-1),interleukin-1β(IL-1β),and IL-18 in pancreatic tissue,and the expression of NLRP3 was observed by immunofluorescence(IF). The results showed that,compared with the normal group,the model group had increased body weight,pancreas-to-weight ratio,GSP,FBG,FINS,and HOMA-IR,distorted and inflammatoryinfiltrated islet cells,and unclear boundary between islet cells and acinus cells. There was a significant rise in the protein expressions of TNF-α,NF-κBp65 and IL-18,and the expression of related proteins in pancreatic tissue was markedly elevated. Compared with the conditions in the model group,the body weight,pancreas-toweight ratio,GSP,FBG,and FINS were significantly lowered in the metformin group and PTR aqueous extract groups. Additionally,more islet cells were intact,with obvious boundaries and greatly reduced inflammatory infiltration,and the protein expressions of TNF-α,NF-κBp65,and IL-18 as well as the expression of related proteins in pancreatic tissue dropped in the administration groups compared with those in the model group. In conclusion,PTR aqueous extract can lessen the inflammatory damage of islet cells,decrease insulin resistance,and alleviate the symptoms of type 2 diabetes mellitus. The mechanism may be related to the suppression of the NLRP3 inflammasome pathway and the release of the downstream inflammatory cytokines IL-1β and IL-18.
Keywords:Puerariae thomsonii Radix;type 2 diabetes mellitus;islet cells;inflammatory damage;NODlike receptor protein 3(NLRP3)inflammasome
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