| Aim: To investigate the protective effects of Tea Polyphenol (TP) on cardiac hypertrophy and cell injury in cultured myocardium cells. Methods: Cardiac hypertrophy models of rats induced by CAA (coarctation of abdominal aorta) and mice induced by continued administration of Isoprenaline (Iso) were used. The H2O2-induced myocardial cell injury in vitro was used as well. RT-PCR was used to determine the expression of PPAR α (peroxisome proliferator activated receptors α ) which is related to cardiac hypertrophy. Results:1. After administration of TP for 5 wks, the cardiac weight indexes and BP were significantly decreased compared with that in the CAA group (P<0.05, P<0.01) , the increase of serum SOD activity and decrease of serum MDA content were found (P<0.05, P<0.01) , the contents of FFA in serum and myocardial tissue were decreased (P<0.01 ) . Also, Na+-K+-ATPase activity in myocardial tissue was elevated in TP groups (PO.01) . At the same time the hydroxyproline content and the hypertrophic myocardial cells and disorder fibril were reduced and abated respectively after administration of TP (PO.01) . 2.After administration of TP for 2 wks, the 'cardiac hypertrophy fatigue' which can be seen from the electrocardiograms and the cardiac weight indexes were decreased (P<0.05, P<0.01) . There were an increase in serum SOD activity, a decrease in serum MDA, LDH, CPK contents and an increase in NO content (P<0.05, P<0.01) . 3.The injury ofmyocardium cells induced by H2O2 when incubated TP with cells was reduced (P<0.01), and LDH release, decreased CP<0.05, P<0.0l) . The [Ca2+]i overload induced by H2O2 was prevented by TP (PO.05, PO.01) . 4. TP can elevate the expression of PPAR a mRNA in mycardial tissue CP<0.05, PO.01). Conclusion: TP could inhibit the cardiac hypertrophy in rats and mice and had protective effects on cultured neonatal rat heart cells. These effects of TP were related to scavenging oxygen free radical, decreasing blood pressure, blocking calcium overload, improving the energy metabolism and increasing PPAR a mRNA expression. |