These data further support the R The HA-1077 ROCK inhibitor amajor of hyperglycemia Chemistry. It has been shown that high blood sugar levels may be increased production of ROS hen What diabetic cardiomyopathy. Antioxidants reverse k Nnten, high glucose-induced cardiac Sch To. In this study, Tiron to scavenge ROS in sufficiently high concentration also attenuated Expression of the M2 mAChR and phosphorylated GATA RIGHTS level by 4 high glucose treatment increased ht. A r The intracellular Ren ROS in B Here expression of M2 mAChR and increase in phospho GATA 4 can therefore be taken into consideration in cardiac cells. GATA 4 is found in heart muscle cells and regulates many genes specific terms such as cardiac ANF, beta type natriuretic peptide, cha Non-myosin heavy angiotensin II and endothelin receptor type IA 1.We observed that expression of M2 mAChR in STZ-diabetic rats increased ht and the ratio changed ratio of phosphorylated GATA 4 and GATA 4 in the kernel with the correct blood sugar GE. In addition, the high induced increase in glucose, the expression of M2 mAChR siRNA of GATA 4 was reversed. Thus, the placement of GATA 4 in the high glucose-induced h Here expression of M2 mAChR reliably, precious metals,. It is known rdern that high blood pressure or stimulation with isoproterenol, phenylephrine or endothelin k Can GATA 4 to up theMEK / ERK activation to GATA 4 serine105 phosphorylation of p38 for a gr Ere binding of GATA 4 in the region f promoter for erh increase the Transkriptionsaktivit t. In this study, PD98059 blocked in a concentration sufficient to MEK / ERK inhibit the high serine 105 phosphorylation induced GATA-4 glucose units and suppresses the expression of M2 mAChR. Phenylephrine acts asalso known to help regulate the number of kidney cells with an induction and repair of renal injury.13 two EMT Dipeptidy and apoptosis are important mechanisms of kidney damage Ending, but there were few studies to determine whether an L Sion is induced Renal function is associated EMTand / or apoptosis of renal tubular cells. In this study, we investigated whether induced in the EMT and apoptosis in cultured renal proximal r Hrenf Shaped cells, and examined the m Matched paths of intracellular Ren signaling for the ph Phenotypic transition is induced, and / or cell death, kidney . Materials and methods All chemicals and reagents were cell culture plates obtained from Sigma Aldrich, St. Louis, MO, USA and Nunc Labware, unless otherwise indicated. Cell culture rat renal Tubul Re epithelial cells were obtained from the American Type Culture Collection. NRK 52E cells were cultured in Dulbecco’s modified Eagle medium with 5% f Fetal calf serum K And 60 mg / ml penicillin erg Complements. The cells were incubated at 371C in a humidified 5% CO2/95% Luftatmosph Kept re incubator. A fresh growth medium was added to the cells every 2 days until the cells a confluence adequate for each experiment. Cytotoxicity t cytotoxicity The SI tstest in NRK 52E cells was determined by the amount of leakage of lactate dehydrogenase in the medium at 48, 72 and 96 h stimulation with the LDH cytotoxicity t detection kits. The cytotoxicity t was released as a percentage of LDH from the cells is Candesartan stimulated to expressed LDH from cell lysates as a whole. Each data set was determined in triplicate. Cell proliferation assay: thymidine incorporation assay was cultured NRK cell.