2011Wuhan Daxue xuebao. Yixue banRequires access

Effects of LY333531 on Antioxidant State and Myocardial NADPH Oxidase in Early Diabetic Rats

Zhengyuan Xia

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Abstract

Objective: To explore the effects of PKC-β inhibitor LY333531 on myocardial NADPH oxidase in early diabetic rats.Methods: Twenty-four male SD rats were randomly assigned to control group(NC),diabetic group(DM) and diabetic group with LY333531(LY) treatment for four weeks.The levels of 15-F2t-Isoprostane and total antioxidant concentration in plasma and heart tissues were assessed by Reagent kit.Morphological changes of cardiomyocytes were observed under light microscope with hematoxylin-eosin staining.The subunits P22phox,P67phox and gP91phox of NADPH oxidase were analyzed by Western blot.Results: The structure of cardiac tissues in DM group was disordered,LY treatment made it close to normal.The 15-F2t-Isoprostane levels and total antioxidant concentrations in plasma and heart tissues,the protein expression of P22phoxand gP91phox,and the membrane translocation of P67phox were significantly increased in diabetic group as compared to control group(all P0.05).LY treatment decreased the levels of 15-F2t-Isoprostane in plasma and heart tissues,as well as plasma total antioxidant concentration,P22phox expression,and membrane translocation of P67phox as compared to control group(P0.05),but there was not a significant change in gP91phox expression.Conclusion: The LY333531 may protect diabetic myocardium from oxidative injury through inhibiting NADPH oxidase activation and expression.

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What this paper is about

Objective: To explore the effects of PKC-β inhibitor LY333531 on myocardial NADPH oxidase in early diabetic rats.Methods: Twenty-four male SD rats were randomly assigned to control group(NC),diabetic group(DM) and diabetic group with LY333531(LY) treatment for four weeks.The levels of 15-F2t-Isoprostane and total antioxidant concentration in plasma and heart tissues were assessed by Reagent kit.Morphological changes of cardiomyocytes were observed under light microscope with hematoxylin-eosin staining.The subunits P22phox,P67phox and gP91phox of NADPH oxidase were analyzed by Western blot.Results: The structure of cardiac tissues in DM group was disordered,LY treatment made it close to normal.The 15-F2t-Isoprostane levels and total antioxidant concentrations in plasma and heart tissues,the protein expression of P22phoxand gP91phox,and the membrane translocation of P67phox were significantly increased in diabetic group as compared to control group(all P0.05).LY treatment decreased the levels of 15-F2t-Isoprostane in plasma and heart tissues,as well as plasma total antioxidant concentration,P22phox expression,and membrane translocation of P67phox as compared to control group(P0.05),but there was not a significant change in gP91phox expression.Conclusion: The LY333531 may protect diabetic myocardium from oxidative injury through inhibiting NADPH oxidase activation and expression.

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Available abstract

Objective: To explore the effects of PKC-β inhibitor LY333531 on myocardial NADPH oxidase in early diabetic rats.Methods: Twenty-four male SD rats were randomly assigned to control group(NC),diabetic group(DM) and diabetic group with LY333531(LY) treatment for four weeks.The levels of 15-F2t-Isoprostane and total antioxidant concentration in plasma and heart tissues were assessed by Reagent kit.Morphological changes of cardiomyocytes were observed under light microscope with hematoxylin-eosin staining.The subunits P22phox,P67phox and gP91phox of NADPH oxidase were analyzed by Western blot.Results: The structure of cardiac tissues in DM group was disordered,LY treatment made it close to normal.The 15-F2t-Isoprostane levels and total antioxidant concentrations in plasma and heart tissues,the protein expression of P22phoxand gP91phox,and the membrane translocation of P67phox were significantly increased in diabetic group as compared to control group(all P0.05).LY treatment decreased the levels of 15-F2t-Isoprostane in plasma and heart tissues,as well as plasma total antioxidant concentration,P22phox expression,and membrane translocation of P67phox as compared to control group(P0.05),but there was not a significant change in gP91phox expression.Conclusion: The LY333531 may protect diabetic myocardium from oxidative injury through inhibiting NADPH oxidase activation and expression.

Key concepts: P22phox, NADPH oxidase, Internal medicine, Antioxidant, Diabetes mellitus, Endocrinology, Diabetic cardiomyopathy, Western blot

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Effects of LY333531 on Antioxidant State and Myocardial NADPH Oxidase in Early Diabetic Rats — Research Paper | ScholarLens