Investigation of the retinal function and pathogenesis in diabetic retinopathy

1.Human research·The retinal blood flow may decrease in the early phase but increase in the late phase after the onset of diabetes mellitus(In Submission)。·The increased RBF may predict development of diabetic retinopathy in patients with type 2diabetes(In Submission)。·The plasma level of NO increases in patients with type 2 diabetic patients。(Japanese J Ophthalmol，2006)·Blockade of angiotensin type II receptor did not change retinal blood flow in healthy subjects(In Submission)。·Vascular endothelial dysfunction may be involved in the pathogenesis of interferon-induced retinopathy in patients with chronic hepatitis C.(Invest Ophthalmol Vis Sci，2007)·2.In vivo animal study·Nitric oxide contributes to RBF recovery after hyperoxia，probably through the action of endothelial NOS via the ETB eptor in the vascular endothelium of the retinal arterioles，suggesting that the BF resved to endothelia of the retinal arterioles(in su…More bmission)。·Acute hyperglycemia significantly reduced the endothelial-dependent BK-induced increase in vessel diameter，bleed velocity and retinal blood flow，suggesting that hyperglycemia per se may induce the acute endothelial dysfunction of retinal arteries。(In Submission)。·3.体外animal study·Simvastatin elicits mainly an endothelium-dependent，NO-mediated dilation of retinal arterioles via activation of guanylyl cyclase(Invest Ophthalmol Vis Sci，2007)·Resveratrol elicits endothelium-dependent and-independent dilation of retinal arterioles。Endothelium-dependent dilation is mediated by the released NO，probably via NO synthase(NOS)activation by the ERK pathway and the subsequent activation of soluble guanylyl cyclase。(Invest Ophthalmol Vis Sci，2007)·CRP inhibits endothelium-dependent NO-mediated dilation in retinal arterioles by producing superoxide from NAD(P)H oxidase，which appears to be linked with p38 kinase and RhoA/Rho-kinase activation。(Invest Ophthalmol Vis Sci，2008)Less

1. Human research・The retinal blood flow may decrease in the early phase but increase in the late phase after the onset of diabetes mellitus (in submission).・The increased RBF may predict development of diabetic retinopathy in patients with type 2 diabetes (in submission).・The plasma level of NO increases in patients with type 2 diabetic patients. (Japanese J Ophthalmol, 2006)・Blockade of angiotensin type II receptor did not change retinal blood flow in healthy subjects (in submission).・Vascular endothelial dysfunction may be involved in the pathogenesis of interferon-induced retinopathy in patients with chronic hepatitis C. (Invest Ophthalmol Vis Sci, 2007)・2. In vivo animal study・Nitric oxide contributes to RBF recovery after hyperoxia, probably through the action of endothelial NOS via the ETB receptor in the vascular endothelium of the retinal arterioles, suggesting that the RBF response to hyperoxia may be used to evaluate the endothelial function of the retinal arterioles. (in su … More bmission).・Acute hyperglycemia significantly reduced the endothelial-dependent BK-induced increase in vessel diameter, bleed velocity and retinal blood flow, suggesting that hyperglycemia per se may induce the acute endothelial dysfunction of retinal arteries. (in submission).・3. in vitro animal study・Simvastatin elicits mainly an endothelium-dependent, NO-mediated dilation of retinal arterioles via activation of guanylyl cyclase (Invest Ophthalmol Vis Sci, 2007)・Resveratrol elicits endothelium-dependent and-independent dilation of retinal arterioles. Endothelium-dependent dilation is mediated by the released NO, probably via NO synthase (NOS) activation by the ERK pathway and the subsequent activation of soluble guanylyl cyclase. (Invest Ophthalmol Vis Sci, 2007)・CRP inhibits endothelium-dependent NO-mediated dilation in retinal arterioles by producing superoxide from NAD(P)H oxidase, which appears to be linked with p38 kinase and RhoA/Rho-kinase activation. (Invest Ophthalmol Vis Sci, 2008) Less