Influence of overexpression of SOCS2 on cells of DN rat

Objective: To explore the influence and mechanism of overexpression of SOCS2 on diabetic nephropathy(DN) rats and cells. Methods: 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 DNAd-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. Results: 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. Conclusions: 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.