The potential mechanism of INHBC and CSF1R in diabetic nephropathy.

Abstract

The aim of this study was to research the potential mechanism of INHBC and CSF1R in diabetic nephropathy. 30 SD rats were selected and randomly divided into Con group, Sham group, and DN group. In the DN group, intraperitoneal injection of the streptozotocin-citrate solution was conducted to construct the DN model. In the Sham group, intraperitoneal injection of equal citrate solution was conducted. The Con group did not do anything. After successful modeling, blood glucose, insulin, biochemical indexes, and levels of inflammatory cytokines in blood samples were detected. The expression levels of INHBC, CSF1R, apoptosis-related proteins and IGF-1 were detected by Western blot. MRNA expression levels of INHBC, CSF1R, IGF-1 and inflammatory cytokines were detected by qPCR. Compared with the Con group, the expression levels of blood glucose, insulin, biochemical indexes, INHBC, CSF1R, IGF-1, IL-6, TNF-α and Bcl2 increased in the DN group, while the expression levels of IL-10, Caspase 3, Caspase 9, and Bax decreased. INHBC mRNA was positively correlated with IGF-1 mRNA. CSF1R was negatively correlated with Caspase 3, Caspase 9, Bax, and IL-10, and positively correlated with IL-6, TNF-α, and Bcl2. NHBC and CSF1R induced the secretion of IL-6 and TNF-α, inhibited the production of IL-10, inhibited apoptosis of cells, and promoted the proliferation of renal cells during DN disease. Therefore, INHBC and CSF1R can be used as target objects of DN treatment strategies.