TLR6与MyD88在小鼠肥胖发生过程中的作用机制研究
Mechanisms of the Role of TLR6 and MyD88 in the Development of Obesity in Mice

目的：探究Toll样受体6 (TLR6)和髓样分化因子88 (MyD88)在肥胖发生发展中发挥的作用。方法：C57BL/6J雄性小鼠20只，随机分为对照组和模型组。对照组给予普通饲料喂养，模型组给予高脂饲料喂养。12周后称重并提取小鼠腹股沟脂肪组织；Western blot检测各组小鼠脂肪组织中TLR6、髓样分化因子88 (MyD88)蛋白表达。结果：肥胖小鼠腹肌沟脂肪组织切片显示脂肪细胞数量增多，间质内可见多量巨噬细胞，TLR6和Myd88蛋白在肥胖小鼠脂肪组织中表达增加。结论：TLR6及Myd88可能通过升高脂肪组织的炎症水平参与了小鼠肥胖的发生。
Objective: To investigate the roles played by Toll-like receptor 6 (TLR6) and myeloid differentiation factor 88 (MyD88) in the development of obesity. Methods: Twenty C57BL/6J male mice were ran-domly divided into control and model groups. The control group was fed standard chow, and the model group was fed high-fat food. Twelve weeks later, the inguinal adipose tissues of the mice were weighed and extracted; the expression of TLR6 and MyD88 in the fatty tissues of each group was detected by Western blot. Results: Groin adipose tissue sections of obese mice showed an increase in the number of adipocytes and a high number of macrophages in the interstitium and increased expression of TLR6 and Myd88 proteins in the adipose tissue of obese mice. Conclusion: TLR6 and Myd88 may be involved in developing obesity in mice by elevating the level of inflammation in adi-pose tissue.