期刊文献+

牙周炎对肥胖小鼠炎症因子、肾纤维化的影响

Effects of periodontitis on inflammatory factors and renal fibrosis in obese mice
下载PDF
导出
摘要 目的:初步探索牙周炎对肥胖小鼠炎症因子、肾损伤的影响。方法:采用高、低脂饲料诱导小鼠肥胖合并牙周炎的模型,分为高脂牙周炎组(High+Pre)、高脂非牙周炎组(High+NCPre)、低脂牙周炎组(Low+Pre)、低脂非牙周炎组(Low+NCPre);观察小鼠血清总蛋白、白蛋白、肌酐含量的变化;采用免疫印迹试验(Western blot)检测TGF-β1/Samd6信号通路相关蛋白、基质金属蛋白酶(matrixmetalloprotease,MMP)-2、MMP-9、金属蛋白酶组织抑制因子(tissue inhibitor of metalloproteinases-1,TIMP-1)的蛋白水平;应用酶联免疫吸附测定法(ELISA)检测肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)、白细胞介素-6(interleukin-6,IL-6)水平的变化。结果:高脂饲喂小鼠的体重第20周已达显著肥胖;与Low+NCPre组相比,High+NCPre组和High+Pre组小鼠血清中总蛋白、白蛋白显著降低(P <0.05),肾组织MMP-2、MMP-9蛋白含量显著下调(P <0.05),血清肌酐、TNF-α、IL-6显著升高(P <0.05),肾组织中TIMP-1蛋白水平显著增加(P <0.05),促进肾组织TGF-β1蛋白表达(P <0.05),抑制肾组织Samd6、E-cadherin蛋白分泌(P <0.05);与High+NCPre组相比,High+Pre小鼠血清中总蛋白、白蛋白显著降低(P <0.05),抑制炎症因子TNF-α、IL-6、MMP-2、MMP-9蛋白表达水平(P <0.05),血清肌酐、肾组织TIMP-1显著增加(P <0.05),肾组织TGF-β1蛋白显著上调(P <0.05),肾组织Samd6、E-cadherin蛋白显著下调(P <0.05)。结论:牙周炎加重肥胖小鼠肾损伤,其可能通过影响TGF-β1/Samd6信号通路促进肾纤维化,抑制细胞外基质降解,促进上皮间质转化。 Objective:This study aims to investigate the effect of inflammatory factors on renal injury in periodontitis model of mice.Methods:High or low fat diet-induced periodontitis models of mice were established.Mice were divided into high fat diet without periodontitis group(High+NCPre),high fat diet with periodontitis group(High+Pre),low fat diet with periodontitis group(Low+Pre),low fat diet without periodontitis group(low+NCPre).The changes of serum total protein,albumin and creatinine in mice were observed.The protein levels of TGF-β1/Samd6 signaling pathway related proteins,MMP-2,MMP-9 and TIMP-1 were detected by Western blot.Changes of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)levels were detected by enzyme linked immunosorbent assay(ELISA).Results:Mice fed with high fat diet were significant obesity at the 20 th week.Compared with those in Low+NCPre group,the levels of total protein and albumin in serum were significantly decreased in High+NCPre group and High+Pre group(P<0.05);MMP-2 and MMP-9 protein expression in kidney were significantly decreased(P<0.05);serum creatinine,TNF-αand IL-6 were increased(P<0.05);The TIMP-1 protein expression in kidney was significantly increased in High+NCPre group and High+Pre group(P<0.05).The expression of TGF-β1 protein(P<0.05)was increased,levels of Samd6 and E-cadherin protein were inhibited in kidney of High+NCPre group and High+Pre group(P<0.05).Compared with those in High+NCPre group,total protein and albumin in High+Pre group were significantly decreased(P<0.05);inflammatory factor levels of TNF-αand IL-6,MMP-2 and MMP-9 protein expression decreased;serum creatinine,TGF-β1 and TIMP-1 proteins in kidney increased(P<0.05);expression of Samd6 and E-cadherin proteins in kidney decreased(P<0.05).Conclusion:Periodontitis aggravates the renal injury of obese mice,which may promote renal fibrosis,inhibit the degradation of extracellular matrix,and promote the process of epithelial-mesenchymal transition by regulating TGF-β1/Samd6 signaling pathway.
作者 赵璐 张彦 顾敏 Zhao Lu;Zhang Yan;Gu Min(Department of Stomatology,First People's Hospital of Changzhou City,Changzhou 213000,China)
出处 《南京医科大学学报(自然科学版)》 CAS CSCD 北大核心 2019年第9期1383-1388,共6页 Journal of Nanjing Medical University(Natural Sciences)
基金 常州市卫生和计划生育委员会项目资金资助(WZ201704) 常州市卫计委青年人才科技项目(QN201708)
关键词 牙周炎 肥胖小鼠 EMT TGF-β1/Samd6 periodontitis obese mice EMT TGF-β1/Samd6
  • 相关文献

参考文献4

二级参考文献25

  • 1张浩,刘伏友,彭佑铭,刘映红.TGF-β_1对人腹膜间皮细胞纤溶酶原激活物抑制剂-1的影响[J].医学临床研究,2004,21(8):864-867. 被引量:5
  • 2任国亨,王成,张媛媛.牙周基础治疗后龈沟液中TNF-α的变化[J].实用医学杂志,2006,22(10):1146-1147. 被引量:12
  • 3Jeremy W Tomlinson, Paul M Stewart. Mechanisms of Disease: selective inhibition of 1113-hydroxysteroid dehydrogenase type 1 as a novel treatment for the metabolic syndrome [J]. Nat Clin Pract Endocrinol Metab, 2005,1 (2) :92-99 被引量:1
  • 4Peteris Alberts,Cecilia Nilsson, Go Ran Selen,et al. Selective Inhibition of 11β-Hy droxysteroid Dehydrogenase Type 1 Improves Hepatic Insulin Sensitivity in Hyperglycemic Mice Strains [J]. Endocrinology,2003,144 ( 11 ) : 4755-4762 被引量:1
  • 5Masuzaki H,Flier JS. Tissue-specific glucocorticoid reactivating enzyme, 11 beta-hydroxysteroid dehy drogenase type 1 (11 beta-HSD1)-a promising drug target for the treatment of metabolic syndrome [J]. Curr Drug Targets Immune Endocr Metabol Disord, 2003,3 (4) : 255 -262 被引量:1
  • 6Alberts P,Engblom L,Edling N,et al. Selective inhibition of 11β-hydroxysteroid dehydrogenase type 1 decreases blood glucose concentrations in hyperglycaemic mice[J]. Diabetologia, 2002,45 ( 11 ) : 1528-1532 被引量:1
  • 7Clement K,Langin D. Regulation of inflammation-related genes in human adipose tissue [J]. J Intern Med, 2007,262 (4) : 422-430 被引量:1
  • 8Wang SJY,Birtles S,J de Schoolmeester,et al. Inhibition of 11β-hydroxysteroid dehydrogenase type 1 reduces food intake and weight gain but maintains energy expenditure in diet-induced obese mice [J]. Diabetologia,2006,49 (6) : 1333-1337 被引量:1
  • 9James S Gilmour,Agnes E Coutinho,Jean-Francois Cailhier, et al. Local Amplification of Glucocorticoids by 11β- Hydroxysteroid Dehydrogenase Type 1 Promotes Macrophage Phagocytosis of Apoptotic Leukocytes [J]. The Journal of Immunology, 2006,176 (12) : 7605-7611 被引量:1
  • 10Bujalska I J, Gathercole LL, Tomlinson JW, et al. A novel selective 11beta-hydroxysteroid dehydrogenase type 1 inhibitor prevents human adipogenesis [J]. J Endocrinol, 2008,197(2) :297-307 被引量:1

共引文献18

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部