Baicalin Inhibits Kidney Inflammation In Mice With Diabetic Nephropathy By Modulating Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

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 C57BU6J 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-alpha, and interleukin-1 beta 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.