RESUMEN
AIM: To investigate the role of Trp3 in the Ca2+ influx induced by α1B-AR in HEK293 cells and the effect of tyrosine kinase on it. METHODS: With lipofect AMINE2000 reagent, hTrp3 cDNA was transfected to HEK293 cells and α1B-HEK293 cells respectively. The expression of Trp3 was examined by Western blot. With Fura-2/AM spectrophoto- fluorometry, Ca2+ influx was determined. RESULTS: HTrp3 was expressed endogenously in HEK293 cells, and the expression increased in hTrp3-transfected-cells. Compared with untransfected cells, transfection of hTrp3 cDNA increased Ca2+ influx induced by α1B-AR (P0.05). 5-30 μmol · L-1 genistein inhibited Ca2+ influx induced by α1B-AR in hTrp3 cDNA -transfected cells and the maximum inhibitory rate was (75.2 ± 12.6)%. CONCLUSION: Transfection of hTrp3 cDNA increased Ca2+ influx induced by α1B-AR in HEK293 cells. This process was regulated by tyrosine kinase.
RESUMEN
To observe the effects of total flavones of Metasequoia glyptostroboides Hu et Cheng (TFM) on volume-overload cardiac hypertrophy and the expression of c-Fos protein in rat. Methods Volume-overload cardiac hypertrophy of rat was induced by aortocaval shunts. The rats were given ig TFM (400, 40 and 4 mg/kg/d). c-Fos protein in the ventricles were measured by immunocytochemical study. Results TFM at the above dosage decreased heart weight and contents of RNA and protein in the myocardium, inhibited the expression of c-Fos protein in the ventricles. Conclusion TFM can prevent volume-overload cardiac hypertrophy in rats. The inhibitory effects on the expression of c-Fos protein may be its mechanism in the molecular level.