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Objectives To investigate the effects of angiotensinII (AngII) and angiotensin-(1-7) [Ang-(1-7)] on scavenger receptor class B type1 (SR-BI), ATP-binding cassette transporter A1 (ABCA1) and cholesterol efflux in THP-1 derived foam cells. Methods Human monocytic cell line (THP-1) was induced intomacrophages by100 nmol/L phorbol myristate acetate (PMA) for 48h, and treated with ox-LDL to construct the foam cells, then were randomly allocated into five groups: control group, AngII group,Ang-(1-7) group, Ang-(1-7) + AngII groupand AngII + Ang-(1-7) + A-779 group. Them RNA and protein expression of SR-BI, ABCA1were determinded by RT-PCR and Westernblot, the intracellular cholesterol efflux rate was detected by liquid scintillator. Results Compared with the control group, AngII decreasedSR-BI andABCA1 in both protein and mRNA, and inhibited the cholesterol efflux ( P P P Conclusions In THP-1 derived foam cells, Ang-(1-7) via its specific receptor MAS attenuates the reduction of the expression of SR-BI and ABCA1 induced by AngII, and increases the cholesterol efflux.

Objectives To observe effects of valsartan on expression of gp130 in cardiac hypertrophy rat induced by Ang II. Methods Neonatal rat cardiomyocyte induced by Ang II into cardiac hypertrophy, and cultivated with different concentrentions of valsartan, used phase contrast microscope to measure transdiameter of cardiomyocyte, the protein synthesis rate was measured by 3H-leucine incorporation; The expression of gp130 mRNA and protein were determined by reverse transcription-polymerase chain reaction (RT- PCR) and western-blot. Results Compared with the control group, myocardial fibre diameter and 3 H-leucine incorporation increased in Ang II group ( P 3 H-leucine incorporation significantly decreased in valsartan + Ang II group ( P Conclusions Valsartan dose-dependently inhibited the expression of gp130 in hypertrophy myocardial rat induced by Ang II, postponed the development of myocardial hypertrophy, and played a important role to protect myocardial cell.