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Effect of SOCS1 on diabetic renal injury through regulating TLR signaling pathway

X-Y Wu1, J Yu, H-M Tian

  • 1Department of Endocrinology and Metabolism, West China Hospital, Sichuan University, Chengdu, China. hmtiann999@126.com.

European Review for Medical and Pharmacological Sciences
|October 11, 2019
PubMed
Abstract

Insights

Suppressor of cytokine signaling 1 (SOCS1) protects against diabetic nephropathy (DN) by inhibiting the Toll-like receptor (TLR) pathway. Upregulating SOCS1 expression in rats reduced kidney injury and inflammation, suggesting SOCS1 as a potential therapeutic target for DN.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Diabetic nephropathy (DN) is a major complication of diabetes, leading to significant renal injury.
  • The Toll-like receptor (TLR) signaling pathway plays a crucial role in mediating inflammation and injury in DN.
  • Suppressor of cytokine signaling 1 (SOCS1) is a key regulator of cytokine signaling and inflammation.

Purpose of the Study:

  • To investigate the therapeutic effect of SOCS1 on diabetic nephropathy (DN)-induced renal injury.
  • To elucidate the role of SOCS1 in regulating the Toll-like receptor (TLR) signaling pathway in DN.
  • To explore SOCS1 as a potential therapeutic target for DN.

Main Methods:

  • Diabetic nephropathy (DN) model established in Sprague-Dawley rats using streptozotocin.
  • SOCS1 expression was upregulated in DN rats using lentivirus administration.
  • Renal function (BUN, creatinine), liver function (ALP, ALT), kidney pathology (HE staining), inflammatory markers (ELISA), and TLR pathway gene/protein expression (RT-PCR, Western blotting) were assessed.

Main Results:

  • Upregulation of SOCS1 significantly reduced blood glucose levels, BUN, ALP, ALT, and creatinine in DN rats.
  • SOCS1 overexpression attenuated kidney inflammatory infiltration and glomerular injury.
  • Serum levels of IL-1, INF-γ, and TNF-α, as well as mRNA/protein expression of MyD88, TLR2, and INF-γ, were significantly downregulated in the SOCS1 overexpression group.

Conclusions:

  • SOCS1 effectively ameliorates renal injury in a rat model of diabetic nephropathy (DN).
  • SOCS1 exerts its protective effects by inhibiting the Toll-like receptor (TLR) signaling pathway.
  • SOCS1 represents a promising therapeutic target for the management of DN-related renal complications.

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