Young Investigators' Award Session

Abstract

O576 Cardiac microvascular dysfunction in diabetes and insulin treatment: Role of glucoseinduced PKC-BII activity ZY Yin, LP Wei, HC Wang Xijing Hospital, Xi’an, China, People’s Republic of Topic: Heart disease Purpose: Diabetes mellitus is an independent risk factor for cardiovascular disease and little attention is addressed on PKC-bII in cardiac microvascular dysfunction. Methods: In animal experiment, normal Sprague-Dawley rat, streptozotocin-induced diabetic rat, insulin-treated and physiological saline-treated diabetic rat were administrated with a serial of evaluations including pressure measurements, angiogenesis and permeability observations under electron microscope, histopathologic analysis for cardiac microvascular endothelium cell (CMECs), TUNEL, and Western blotting for PKC-bII. In cell research part, CMECs in four different mediums (normal medium, high-glucose concentration medium, insulin-stimulated and physiological saline-stimulated high-glucose medium) were investigated with MTT, apoptosis, quantitative permeability assessment and Western blotting. Results: 1. Accompanied with more active expression of PKC-bII and higher apoptosis rate in diabetic model, either increased microvascular permeability or pathological angiogenesis is observed, and which is attenuated in certain extent while receiving insulin treatment. 2. Accordant results from cell research were obtained. Compared with normal group, CMECs in high-glucose medium are demonstrated with poor proliferation, more notable apoptosis, increased permeability of cell monolayer, and augmented PKC-bII expression. Insulin-stimulated group poses a midst performance between normal and high-glucose group. Conclusions: Increased PKC-bII activity has been implicated responsible for the pathogenesis of cardiac microvascular dysfunction in diabetes and elevated glucose is sufficient to induce these effects. PKC-bII is indicated to occupy an important position in the whole process of insulin treatment.