Taurine attenuates diabetic nephropathy by suppressing the HMGB1/TLR4/MyD88/NF-κB axis in mice

Inflammation is intimately correlated to diabetic nephropathy (DN) etiology and pathogenesis. The scope of this investigation was to explore possible prophylaxis effects of taurine on DN from the perspective of TLR4/NF-κB signaling transductions and inflammation inhibition. Streptozotocin (STZ) was injected into the tail vein of mice. On the 8th week, serum and kidney tissues were collected, followed by adoption of the microplate method for analyzing creatinine serum/urea nitrogen levels from such tissues. The serum levels of inflammatory factors were detected through ELISA. The activity of MPO in renal tissue was detected by colorimetry. The expression levels of the fibrosis marker α-SMA in mouse kidney tissues and the protein markers related to the glomerular podocytes (Nephrin, Synaptopodin, and F-actin), as well as Ly6G and CD68 in the kidney tissues, were detected by IF. Western blot was employed for analyzing protein expression levels of inflammatory factors and TLR4/NF-κB pathway proteins in renal tissue. Taurine was effective in reducing blood glucose levels, inhibiting weight loss and kidney index changes in diabetic mice, inhibiting inflammatory cell infiltration by reducing MPO activity and overexpression of CD68 and MCP-1, reducing the serum creatinine and urea nitrogen levels, effectively regulating serum/renal tissue levels of IL-6, IL-1β, and TNF-α and effectively regulating protein expression of inflammatory factors in renal tissues, and restoring the expression level of glomerular podocyte marker proteins. Taurine can effectively inhibit inflammatory reactions and fibrosis, repair the glomerular filtration membrane, and protect normal renal function, together with inhibiting DN pathogenesis.