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目的检测Ⅱ型糖尿病(T2DM)C57BL/6小鼠外周血及脾脏中白细胞介素-17(IL-17)、β转化生长因子(TGF-β)、白细胞介素-6(IL-6)的变化。方法 C57BL/6小鼠糖尿病造模成功后,于d 3、d 9、d 15、d 21取血及脾脏,用ELISA方法检测小鼠外周血中IL-17、TGF-β、IL-6水平变化及用RT-PCR检测小鼠脾脏IL-17、TGF-β、IL-6 m RNA的表达情况。结果小鼠造模成功后的d 3、d 9、d 15、d 21,外周血IL-17水平在d 3、d 9高于对照组(P<0.05);TGF-β水平在d 3高于对照组(P<0.05),随时间的增长呈下降趋势;IL-6水平呈上升趋势,在d 9、d15高于对照组(P<0.05)。脾脏中IL-17在d 3、d 9高于对照组(P<0.05);TGF-β表达呈下降趋势,在d 3高于对照组(P<0.05);IL-6表达呈上升趋势,在d 9、d 15、d 21高于对照组(P<0.05)。结论Ⅱ型糖尿病C57BL/6小鼠模型中IL-17、TGF-β的表达在造模早期呈升高趋势,IL-6的表达高于对照组,并在d 15达到高峰。该研究结果为Th17亚群在T2DM发生发展进程中发挥的免疫学作用提供了动态的理论数据,并为临床免疫治疗提供理论基础。
Objective To detect the levels of interleukin-17, β-transforming growth factor (TGF-β) and interleukin-6 (IL-6) in peripheral blood and spleen of type 2 diabetes mellitus (T2DM) Variety. Methods After successful diabetes model in C57BL / 6 mice, blood and spleen were collected on d 3, d 9, d 15 and d 21, and the levels of IL-17, TGF-β and IL-6 in peripheral blood were measured by ELISA The expression of IL-17, TGF-β, IL-6 m RNA in spleen of mice was detected by RT-PCR. Results The levels of d 3, d 9, d 15, d 21 and peripheral blood IL-17 in d 3 and d 9 were significantly higher than those in control group (P <0.05) after successful modeling. The levels of TGF- In the control group (P <0.05), the level of IL-6 showed a decreasing trend with the increase of time. The level of IL-6 showed an upward trend at d 9 and d 15 (P <0.05). IL-17 in the spleen was higher than that in the control group at d 3, d 9 (P <0.05); the expression of TGF-β was down-regulated at d 3 and higher than that in the control group (P <0.05) At d 9, d 15 and d 21 were higher than those in control group (P <0.05). Conclusion The expression of IL-17 and TGF-β in C57BL / 6 mouse model of type Ⅱ diabetes mellitus were increased in the early stage of modeling, and the expression of IL-6 was higher than that in the control group, reaching its peak on d 15. The results provide dynamic theoretical data for the immunological role played by Th17 subtypes in the development of T2DM and provide a theoretical basis for clinical immunotherapy.