Toll样受体2基因敲除减轻1型胶原在高脂饮食诱导的肥胖小鼠脂肪组织的沉积  

Deposition of collagen I in adipose tissue of obese mice was inhibited by toll like receptor 2 knockout

作　　者：张浩强 王茹 宋冰 

机构地区：[1]锦州医科大学附属第一医院内分泌科,121000 [2]锦州医科大学研究生学院,121000

出　　处：《中华内分泌代谢杂志》2017年第5期408-412,共5页Chinese Journal of Endocrinology and Metabolism

基　　金：2013年辽宁省博士启动基金（20131067）;2016年辽宁省自然科学基金（201602308）

摘　　要：目的研究toll样受体2（TLR2，toll like receptor2）基因敲除对高脂饮食诱导的肥胖小鼠脂肪组织I型胶原沉积的影响。方法雄性C57b1／6小鼠和TLR2基因敲除小鼠根据普通饮食或高脂饮食喂养分组并制造肥胖模型。实验结束后Masson染色检测脂肪组织总胶原变化。Western印迹检测TLR2、I型胶原、基质金属蛋白酶1（MMP1，Matrix metalloproteinase1）、MMP2和基质金属蛋白酶组织抑制剂1（TIMP1，Tissue inhibitor of metalloproteinase1）蛋白相对表达量。荧光实时定量PCR检测小鼠脂肪组织I型胶原α1和I型胶原α2mRNA相对表达量。结果高脂饮食小鼠脂肪组织TLR2、总胶原、I型胶原、MMP2和TIMP1蛋白升高；I型胶原α1和I型胶原α2mRNA相对表达量升高，MMP1蛋白相对表达量减少。与肥胖组相比，基因敲除的高脂饮食小鼠脂肪组织总胶原、I型胶原、MMP2和TIMP1蛋白降低；I型胶原α1和I型胶原α2mRNA相对表达量降低，而MMP1蛋白相对表达量升高。结论TLR2基因敲除可能通过TIMP1和MMP1减少了I型胶原在高脂饮食诱导的肥胖小鼠脂肪组织的沉积。Objective To explore the effect of TLR2 on collagen I （ col I ） in adipose tissue of high-fat-diet induced obese mice. Methods Male C57bl/6J mice and TLR2 knockout mice were divided into groups according to high fat diet or normal chow. Total collagen, TLR2, col I , MMP1, MMP2, TIMP1, col I cd mRNA and col I α2 mRNA in adipose tissue were measured at the end of the experiments. Results Total collagen, TLR2, col I , MMP2, TIMP1, col I α1 mRNA, and col I α2 mRNA in adipose tissue increased while MMP1 in adipose tissue decreased in mice with high fat diet. Decreased levels of total collagen, col I , MMP2, TIMP1, col I α1 mRNA and col I α2 mRNA in adipose tissue were detected in TLR2 gene knockout mice with high fat diet. However, there was an increased level of MMP1 in TLR2 gene knockout mice with high fat diet. Conclusion In high-fat-diet induced obese mice, deposition of col I in adipose tissue seems to be alleviated by TLR2 gene knockout via MMP1 and TIMP1.

关 键 词：肥胖症 TOLL样受体2 I型胶原 基质金属蛋白酶1 基质金属蛋白酶组织抑制剂1 

分 类 号：R589.2[医药卫生—内分泌]