Figure 5.

MD2 knockout attenuated diabetes‐induced renal damage and inhibited activation of RAS in mice. MD2 knockout mice (KO), valsartan (Val) ‐treated C57BL/6 mice, and their wild‐type control (WT) developed diabetes (DM), 4 months after STZ injection. (a–e) Kidney/body weight ratio (a), serum creatinine (b), urinary albumin (c), urinary albumin/creatinine ratio (d), Ang II level in kidney tissues (e), and Ang II level in serum (f) were detected by corresponding kits. (g) The kidney tissue mRNA for ACE, renin, and AT₁ receptors were determined by real‐time qPCR assay and normalized to β‐actin. (h) Representative western blot analysis of ACE and phosphorylated MAPKs in kidney tissues. Bar graph shows mean values ± SEM; n = 8 mice per group, *P < .05, significantly different as indicated; ns = not significant. WT‐Ctrl, wild‐type non‐diabetic mice; WT‐DM, wild type diabetic mice; WT‐DM + Val valsartan‐treated diabetic mice; KO‐Ctrl, MD2 knockout nondiabetic mice; KO‐DM, MD2 knockout diabetic mice