Baicalin Inhibits Kidney Inflammation in Mice with Diabetic Nephropathy by Modulating Toll-like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

Abstract

We have explored the effect of baicalin, an anti-inflammatory agent, on the outcome of diabetic nephropathy. To this end, we used 6 weeks old C57BL/6J male diabetic mice exhibiting nephropathy. The treatment with baicalin exhibited significant improvement in the renal function, histopathological changes, and expression of inflammatory markers. Moreover, the expression of interleukin-6, tumor necrosis factor-α, and interleukin-1β in kidney tissue of the mice in baicalin group were significantly downregulated compared to the control group (P ‹ 0.05). The expression of toll-like receptor 4, myeloid differentiation factor 88, and nuclear factor-kappa B proteins in the kidney of baicalin-treated mice were remarkably downregulated compared to the control group. Taken together, we conclude that baicalin may exert its protective effect on kidney by inhibiting inflammation through toll-like receptor 4/nuclear factor-kappa B signaling pathway in mice with diabetic nephropathy.