Here we hypothesized that aqueous garlic homogenate click here may mediate cardioprotection via nitric oxide (NO). Mice were fed with saline and aqueous garlic homogenate (250 and 500 mg kg(-1) day(-1) orally) for 30 days. In another set of experiment, mice were pre-treated with saline, aqueous garlic homogenate (AGH) (250 mg kg(-1)

day(-1) for 30 days), and AGH (30 days) along with L-NAME (20 mg kg(-1) day(-1) i.p. for last 7 days) before inducing acute myocardial infarction by isoproterenol (s.c. injection of isoproterenol 150 mg kg(-1)day(-1) for 2 days) and sacrificed after 48 h. Dose dependent increase in serum NO level was observed after garlic 250 and 500 mg kg(-1) dose feeding. While no change in serum SGPT and SGOT level, a significant decrease in serum LDH level was observed after garlic feeding. Garlic-induced NO formation was further confirmed in human aortic endothelial cells (HAEC). Administration of isoproterenol caused a significant decrease in endogenous antioxidants i.e., myocardial catalase. GSH and GPx activity, and mitochondrial enzyme activities like citrate synthase

and 13 hydroxyacyl CoA dehydrogenase. All those deleterious cardiac changes induced by isoproterenol were PDGFR inhibitor significantly attenuated by garlic homogenate. However this beneficial effect of garlic was blunted when garlic was administered with L-NAME, a nonspecific inhibitor of nitric oxide synthase (NOS). Further, a significant increase in myocardial TBARS and decrease in total antioxidant activity was observed in L-NAME treated group compared to isoproterenol treated group. Administration of L-NAME in mice from control group lowered serum and cardiac NO levels without any change of oxidative stress parameters. In conclusion, our study provides novel evidence that garlic homogenate Progesterone is protective in myocardial infarction

via NO-signaling pathway in mice. (C) 2012 Elsevier Inc. All rights reserved.”
“The members of the HOX transcription factor family are important basic regulators of morphogenesis and development and several HOX proteins have also been identified as essential regulators of physiological and pathologic angiogenesis. HOXC9 is highly expressed in quiescent endothelial cells and keeps the vasculature in a resting state via inhibition of interleukin-8 production. HOXC9 overexpression in zebrafish negatively regulated vascular development which can be rescued by exogenous interleukin-8. The further understanding of the HOXC9-IL-8 signaling axis and the identification of other HOXC9 targets in the vasculature will provide important insights into mechanisms promoting endothelial cell activation during physiological angiogenesis. It will also be beneficial to understand pathophysiological angio genesis regulation and thus provide important new directions for the development of novel anti-angiogenic therapeutic strategies. (Trends Cardiovasc Med 2012;22:7-11) (c) 2012 Elsevier Inc.