Prenatal exposure to testosterone induces cardiac hypertrophy in adult female rats through enhanced Pkcδ expression in cardiac myocytes.

High circulating androgen in women with polycystic ovary syndrome (PCOS) may increase the risk of cardiovascular disease in offspring. The aim of the present study is to investigate whether maternal androgen excess in the rat PCOS model would lead to cardiac hypertrophy in offspring. Maternal testosterone propionate (maternal-TP)-treated adult female offspring displayed cardiac hypertrophy associated with local high cardiac dihydrotestosterone (DHT). The molecular markers of cardiac hypertrophy along with androgen receptor (AR) and PKCδ, were increased in the Maternal-TP group. Treatment of primary neonatal rat ventricular cardiomyocytes (NRCMs) and H9c2 cells with DHT significantly increased cell size and upregulated PKCδ expression, which could be attenuated by AR antagonist. Treatment with phorbol 12-myristate 13-acetate (PMA), a PKC activator, significantly increased cell size and upregulated myh7 level. Rottlerin, that may inhibit PKCδ, significantly reduced the hypertrophic effect of DHT and PMA on NRCMs and H9c2 cells. Chromatin immunoprecipitation revealed that AR could bind to Pkcδ promoter. Our results indicate that prenatal exposure to testosterone may induce cardiac hypertrophy in adult female rats through enhanced Pkcδ expression in cardiac myocytes.

Iron-Catalyzed Regioselective Transfer Hydrogenative Couplings of Unactivated Aldehydes with Simple Alkenes.

An FeBr3 -catalyzed reductive coupling of various aldehydes with alkenes that proceeds through a direct hydride transfer pathway has been developed. With (i) PrOH as the hydrogen donor under mild conditions, previously challenging coupling reactions of unactivated alkyl and aryl aldehydes with simple alkenes, such as styrene derivatives and α-olefins, proceeded smoothly to furnish a diverse range of functionalized alcohols with complete linear regioselectivity.

Effect of peroxisome proliferator-activated receptor gamma ligand. Rosiglitazone on left ventricular remodeling in rats with myocardial infarction.

BACKGROUND: Recent studies have demonstrated that PPARgamma ligands have anti-inflammatory effect which is involved in ventricular remodeling. So we hypothesized that PPARgamma ligand may have beneficial effects on post-infarct ventricular remodeling. METHODS: Experimental myocardial infarction (MI) was induced in SD rats by ligation of the left coronary artery. Twenty-four hours after surgery, survival rats were randomly divided into MI group and Rosiglitazone (MI+Ros) group which would take rosiglitazone 3 mg/kg day for 8 weeks. After 8 weeks treatment, left ventricular hemodynamics were measured and organs were weighed. Myocardial collagen analysis was determined in Van Gieson staining by quantitative morphometry. Myocardial angiotensin II and aldosterone were detected by radioimmunoassay. Myocardial AT1 and AT2 mRNA expression were determined by RT-PCR. RESULTS: Only 1 rat in MI group died of anesthesia at the 8th week. Rosiglitazone treatment could improve left ventricular +/-dp/dt(max), collagen volume fraction and perivascular circumferential area; reduce lung/body mass ratio and liver/body mass ratio; inhibit myocardial angiotensin II and aldosterone; and had no significant effects on myocardial AT1 and AT2 mRNA. Plasma insulin and blood glucose were comparable between two groups. CONCLUSIONS: PPARgamma ligand has neutral effect on mortality and beneficial effect on post-infarct ventricular remodeling, partly by suppressing myocardial angiotensin II and aldosterone, irrespective of plasma insulin and blood glucose level.