论文部分内容阅读
该文探讨了细胞因子信号传导抑制蛋白1(suppressors of cytokine sigmaling 1,SOCS1)在糖尿病小鼠肾小管间质病变中的作用。通过腹腔注射链脲佐菌素(streptozotocin,STZ)诱发糖尿病小鼠模型,于成模后8周给予尾静脉快速注射p EF-FLAG-I/m SOCS1质粒(1 mg/kg),每隔7 d注射一次。于成模后12周收集标本,检测各组动物的血糖、24 h尿蛋白;应用RT-PCR检测肾组织中SOCS1、角蛋白18(cytokeratin,CK18)和α-平滑肌肌动蛋白(α-smooth muscle actin,α-SMA)m RNA的表达;应用免疫组化或Western blot检测SOCS1、CK18、α-SMA和纤维黏连蛋白(fibronectin,FN)的表达;酶联免疫吸附实验检测肾组织中白细胞介素-1β(interleutin-1β,IL-1β)和转化生长因子-β1(transforming growth factor-β1,TGF-β1)的表达;流式细胞术检测肾皮质中巨噬细胞标志蛋白CD68的表达。结果发现,与对照组相比,糖尿病小鼠肾组织中IL-1β、TGF-β1及FN的表达增强,巨噬细胞的数量增多;此外,肾小管上皮细胞自身标志蛋白CK18的表达减少而肌成纤维细胞标志蛋白α-SMA的表达增强。SOCS1质粒转染能降低24 h尿蛋白、抑制肾组织中CD68、IL-1β、TGF-β1和α-SMA的表达,同时部分恢复CK18的表达。结果表明,SOCS1可能通过抑制肾组织炎症反应和肾小管上皮细胞转分化从而缓解糖尿病小鼠肾小管间质病变。
This article explored the role of suppressors of cytokine sigmaling 1 (SOCS1) in tubulointerstitial lesions in diabetic mice. The diabetic mice model was induced by intraperitoneal injection of streptozotocin (STZ), and the p EF-FLAG-I / m SOCS1 plasmid (1 mg / kg) was given to the tail vein 8 weeks after the injection. d injection once. The samples were collected 12 weeks after the operation and the blood glucose and 24 h urinary protein of each group were measured. The expressions of SOCS1, cytokeratin (CK18) and α-smooth muscle actin (α-smooth muscle actin The expressions of SOCS1, CK18, α-SMA and fibronectin (FN) were detected by immunohistochemistry or Western blot. The levels of leukocyte in renal tissue were detected by enzyme-linked immunosorbent assay The expression of interleukin-1β (IL-1β) and transforming growth factor-β1 (TGF-β1) in renal cortex were detected by flow cytometry. The results showed that compared with the control group, the expression of IL-1β, TGF-β1 and FN was increased and the number of macrophages was increased in the kidney of diabetic mice. In addition, the expression of CK18, a marker of renal tubular epithelial cells, The expression of fibroblast marker protein a-SMA is enhanced. SOCS1 plasmid transfection can reduce 24 h urinary protein, inhibit the expression of CD68, IL-1β, TGF-β1 and α-SMA in renal tissue, and partially restore the expression of CK18. The results showed that SOCS1 may alleviate the tubulointerstitial lesions in diabetic mice by inhibiting the inflammatory reaction of renal tissue and the renal tubular epithelial cell transdifferentiation.