Aim:To investigate the effects of angiotensin receptor blocker (ARB) telmisartanon the expression and distribution of protein kinase C (PKC)-α in the kidneys ofdiabetic mice.Methods:Diabetic mice were induced with streptozotocin and agroup of them were randomly selected for treatment with telmisartan.After 6weeks,the expression and localization of PKC-α in the renal cortex,and the outerand inner medulla were assessed by immunohistochemistry and semiquantitativeWestern blotting.In addition,expressions of PKC-α,transforming growth factor-β1 (TGF-β1),and vascular endothelial growth factor (VEGF) in glomeruli weremeasured by semiquantitative immunohistochemistry.Results:Diabetic and nor-mal mice showed similar distributions of PKC-α in the kidneys.The expression ofPKC-α was found in glomeruli,epithelial cells of proximal tubules,and medullary-collecting duct,while not in the medullary and cortical thick ascending limb,andwas different in the epithelial cells of proximal tubules of diabetic nephropathy(DN) mice,PKC-α was mostly translocated from the basement membrane to theapical membrane,whereas it was largely translocated from the apical membrane tothe basement membrane in epithelial cells of the inner medullary-collecting duct.Western blotting detected increased expression of PKC-α in the renal cortex andouter medulla,but not in the inner medulla of DN mice.Enhanced expressions ofPKC-α,TGF-β1,and VEGF were shown in the glomeruli of DN mice,where PKC-αexhibited a correlation to VEGF,but no correlation to TGF-β1.ARB telmisartanattenuated alterations of PKC-α as mentioned earlier in the DN mice.Conclusion:Our findings suggest that PKC-α may play a role in the pathogenesis of DN,andthat the nephroprotective effects of ARB telmisartan may be partly associatedwith its influence on PKC-α. Aim: To investigate the effects of angiotensin receptor blocker (ARB) telmisartanon the expression and distribution of protein kinase C (PKC) -α in the kidneys of diabetic mice. Methods: Diabetic mice were induced with streptozotocin and agroup of them were randomly selected for treatment with telmisartan. After 6 weeks, the expression and localization of PKC-α in the renal cortex, and the outerand inner medulla were assessed by immunohistochemistry and semiquantitative Western blotting. In addition, expressions of PKC-α, transforming growth factor-β1 ), and vascular endothelial growth factor (VEGF) in glomeruli weremeasured by semiquantitative immunohistochemistry. Results: Diabetic and nor-mal mice were similar distributions of PKC-α in the kidneys. The expression of PKC-α was found in glomeruli, epithelial cells of the proximal tubules, and medullary-collecting duct, while not in the medullary and cortical thick ascending limb, and was different in the epithelial cells of proximal tubules of d iabetic nephropathy (DN) mice, PKC-alpha was mostly translocated from the basement membrane to theapical membrane, whereas it was largely translocated from the apical membrane tothe basement membrane in epithelial cells of the inner medullary-collecting duct. Western blotting detected increased expression of PKC-α in the renal cortex andouter medulla, but not in the medulla of DN mice. Enhanced expressions of PKC-α, TGF-β1, and VEGF were shown in the glomeruli of DN mice, where PKC-αexhibited a correlation to VEGF, but no correlation to TGF-β1. ARB telmisartan attenuated alterations of PKC-α as mentioned earlier in the DN mice. Confluence: Our findings suggest that PKC-α may play a role in the pathogenesis of DN, and the effect of the nephroprotective effects of ARB telmisartan may be partly associated with its influence on PKC-α.