肿瘤坏死因子α抑制剂对糖尿病大鼠肾脏的保护作用

    Protective effect of TNF-α inhibitor on diabetic nephropathy in rats

    • 摘要: 目的 探讨肿瘤坏死因子α(TNF-α)抑制剂对糖尿病肾小管间质病变的作用及其相关机制。方法 采用链脲霉素(STZ)诱导建立1型糖尿病大鼠模型,并将大鼠分为模型组(不给予药物治疗)、IgG治疗组(给予IgG 1 mg/kg治疗,每周一次,腹腔注射,治疗12周)和TNF-α抑制剂治疗组(给予阿达木单抗1 mg/kg治疗,每周一次,腹腔注射,治疗12周),另外设立正常对照组。测定各组大鼠肾功能指标、氧化应激指标、炎性因子及炎症小体Nod样受体蛋白3(nod-like receptor protein 3,NLRP3)水平。结果 与IgG治疗组相比,TNF-α抑制剂能够显著减少糖尿病大鼠的白蛋白尿、抑制氧化应激、保护肾小球和肾小管损伤,并减少肾小球和肾小管的NLRP3炎症小体表达(P<0.05)。结论 TNF-α抑制剂可减轻糖尿病肾小管间质病变,其机制可能是通过抑制NLRP3炎性小体的表达来发挥作用。

       

      Abstract: Objective To explore the protective effect of TNF-α inhibitor on diabetic tubulointerstitium damage, and its related mechanism. Methods The rat model of type I diabetes was established by using STZ induction method, and the rats were divided into model group (without medication), IgG treatment group (administered with IgG 1 mg/kg, once per week, intraperitoneally, for 12 weeks), and TNF-α inhibitor group (administered with Humira (adalimumab) injection, once per week, intraperitoneally, for 12 weeks). In addition, the control group was set. Renal function indices, oxidative stress indices, inflammatory factors and NLRP3 inflammasome level were determined. Results Compared with the IgG treatment group, TNF-α inhibitor reduced urinary albumin significantly, inhibited oxidative stress, protected against glomerular and tubular injury, and also reduced expression of NLRP3 inflammasome in the glomeruli and renal tubules (P<0.05). Conclusions TNF-α inhibitor could attenuate diabetic tubulointerstitium damage probably by inhibiting the NLRP3 inflammasome.

       

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