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Diabetic cardiomyopathy is the most common chronic complication of diabetes, the pathological changes mainly in myocardial cell hypertrophy, degeneration, focal necrosis, interstitial accumulation of insoluble collagen, fibrosis, clinical manifestations of early diastolic function insufficiency in the late stage mainly to systolic dysfunction. Research on the pathogenesis of diabetic cardiomyopathy, mainly focused on myocardial cell metabolism, calcium ion transport, and abnormal oxygen free radicals. Related intracellular signal transduction and cell regulation in diabetes research and more attention, the mechanism of disease, excessive activation of diacylglycerol - protein kinase C (DAG-PKC) pathway plays a pivotal role. PKC as a second messenger of the target protein, plays an important regulatory role in myocardial cell morphology and systolic and diastolic function. High blood sugar can cause cell membrane damage by DAG-PKC pathway, inhibition of Na -K > -ATPase enzyme and calcium pump activity, intracellular calcium overload, resulting in the resulting systolic and diastolic dysfunction, eventually leading to heart failure. The increase in the expression of PKC and enhanced activity can be regulated on activation of proto-oncogene gene c-fos expression of c-Jun and other causes ventricular hypertrophy, interstitial fibrosis and left ventricular dysfunction. In this experiment, neonatal rat cardiomyocytes cultured in high glucose as a model, by measuring the diameter of the myocardial cells, beating frequency and PKC-alpha, PKC-beta 2 , the activity of PKC-alpha's (P-PKC-alpha ), PKC-beta 2 of activity (P-PKC-beta 2 ), NF-kappa B and c-fos expression levels, research PKC inhibitor chelerythrine alkali (chelerythrine) on myocardial protection in diabetic cardiomyopathy, and to explore the role of PKC signaling pathway in the pathogenesis of diabetic cardiomyopathy. The purpose of this thesis is: To investigate the protein kinase C inhibitor celandine red base of neonatal rat cardiomyocytes cultured in high glucose morphology and function, as well as protein kinase C (Protein Kinase C, PKC) α, β 2 , nuclear factor-kappa B (Nuclear Factor NF), the level of c-fos expression and activity changes. By the following methods: the establishment of neonatal rat cardiac cell culture models, were randomly divided into low-sugar (5 mmol / L), high glucose (25.5 mmol / L) and high glucose (25.5 mmol / L) of different concentrations white chelerythrine (1 mmol / L, group 8μmol / L) were observed in each group myocardial cells pulse conditions, myocardial cell diameter was measured by Western blot detection of myocardial cells PKC-alpha, PKC-beta 2 , p-PKC-alpha, p The-of PKC-beta 2 , NF-kappa B and c-fos expression levels. Our results: the high glucose myocardial cell beating frequency, cell diameter and PKC-alpha, PKC-beta 2 , p-PKC-alpha, p-PKC-beta 2 NF-kappa B and c-fos expression levels higher than the low-sugar culture group, the difference was statistically significant; different concentrations of PKC inhibitor chelerythrine alkali enables high glucose group myocardial cell beating frequency, cell diameter and PKC-alpha, PKC-beta 2 , p-PKC-alpha, p-PKC-beta 2 , the NF-kappa B and c-fos expression levels reduced by an average and in a concentration-dependent manner. Therefore, we can conclude that: white chelerythrine can inhibit changes in the morphology and function of the neonatal rat myocardial cells induced by high glucose, and inhibition of PKC-alpha, PKC-beta 2 , NF-kappaB and c-fos expression and activity has a protective effect on myocardial cells in high glucose, which may be associated with PKC / NF-kappa B / c-fos pathway.
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