Department of Nephrology, Haerbin Medical University Affiliated First Hospital, China.
Department of Nephrology, Haerbin Medical University Affiliated First Hospital, China.
Asian Pac J Trop Med. 2015 Jul;8(7):583-9. doi: 10.1016/j.apjtm.2015.06.006. Epub 2015 Jul 9.
To explore the influence and mechanism of overexpression of SOCS2 on diabetic nephropathy (DN) rats and cells.
STZ was used to induce male SD rats and SOCS2 was injected into left renal vein. Rats were divided into DN group, DN-Ad-null group and DN-Ad-SOCS2 group. Glucose with high and normal concentration was used to culture HBZY-1 cells and then transfect Ad-SOCS2. HG group, HG-Ad-null group, HG-Ad-SOCS2 group, CG group, CG-Ad-null group, and CG-Ad-SOCS2 group were created. The expression of inflammatory cytokines (MCP-1, TNF-α and IL-6) in kidney tissue of rats, fibrosis related protein (FN, Collagen IV and TGF-β) in kidney tissue and cells of rats, and JAK/STAT signaling pathway related proteins (p-JAK2 and p-STAT3) were tested by western blot. ELISA was used to test the expression of inflammatory cytokines (TNF-α and IL-6) in cells.
The expression of inflammatory cytokines in DN rats (MCP-1, TNF-α and IL-6) and cell (TNF-α and IL-6) were increased (P < 0.01) significantly. However, SOCS2 could decrease the overexpression of mediated inflammatory cytokines in DN animal models and cell models (P < 0.01). The expression of fibrosis related protein in DN rats and cells increased while SOCS2 decreased the overexpression of mediated fibrosis related protein in DN model rats and cells (P < 0.01). The expression of JAK/STAT pathway related protein in both DN rats and cells increased and the JAK/STAT signaling pathway was activated. Yet, SOCS2 obviously suppressed the expression of the JAK/STAT signaling pathway as well as the related proteins (p-JAK2 and p-STAT3) in both DN rats and cells.
The overexpression of SOCS2 can decrease the expression of inflammatory cytokines and fibrosis related proteins in DN rats and cells, and meanwhile suppress the activation of JAK/STAT signaling pathway mediated by DN.
探讨过表达 SOCS2 对糖尿病肾病（DN）大鼠及细胞的影响及机制。
采用 STZ 诱导雄性 SD 大鼠，经左肾静脉注射 SOCS2，将大鼠分为 DN 组、DN-Ad-空载体组和 DN-Ad-SOCS2 组。高糖和正常糖浓度培养 HBZY-1 细胞，转染 Ad-SOCS2，构建 HG 组、HG-Ad-空载体组、HG-Ad-SOCS2 组、CG 组、CG-Ad-空载体组、CG-Ad-SOCS2 组。Western blot 检测大鼠肾组织中炎症因子（MCP-1、TNF-α、IL-6）、纤维化相关蛋白（FN、Collagen IV、TGF-β）及大鼠肾组织和细胞中 JAK/STAT 信号通路相关蛋白（p-JAK2、p-STAT3）的表达，ELISA 检测细胞中炎症因子（TNF-α、IL-6）的表达。
DN 大鼠（MCP-1、TNF-α、IL-6）及细胞（TNF-α、IL-6）中炎症因子表达增加（P<0.01），SOCS2 可降低 DN 动物模型及细胞模型中炎症因子的过表达（P<0.01）。DN 大鼠及细胞纤维化相关蛋白表达增加，SOCS2 降低 DN 模型大鼠及细胞中纤维化相关蛋白的过表达（P<0.01）。DN 大鼠及细胞 JAK/STAT 通路相关蛋白表达增加，JAK/STAT 信号通路被激活，SOCS2 明显抑制 DN 大鼠及细胞 JAK/STAT 信号通路及相关蛋白（p-JAK2、p-STAT3）的表达。
过表达 SOCS2 可降低 DN 大鼠及细胞中炎症因子和纤维化相关蛋白的表达，同时抑制 DN 介导的 JAK/STAT 信号通路的激活。
