Myocardial SO(2) content was detected by high-performance liquid chromatography. GOT (key enzyme for endogenous SO(2) production) activity and gene (GOT1 and GOT2) expressions were measured, and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), hydrogen peroxide, and superoxide radical levels were assayed. SOD
(SOD1 and SOD2) and GSH-Px (GSH-Px1) gene expressions were also detected. The results showed that SO(2) donor at a dose of 85 mg/(kg day) did not impact the cardiac function and structure of rats, but exerted a subtle influence on myocardial redox status. ISO-treated rats exhibited decreased cardiac function, damaged myocardial structures, and downregulated endogenous SO(2)/GOT pathway. Meanwhile, myocardial oxidative stress increased, whereas antioxidative capacity downregulated. Administration of SO(2) markedly improved cardiac selleck kinase inhibitor function and ISO-induced myocardial damage by ameliorating the pathological structure of the
myocardium and the mitochondria. At the same time, myocardial products of oxidative stress decreased, whereas antioxidative capacity increased. These results suggest that downregulation of the endogenous SO(2)/GOT pathway is likely involved in the pathogenesis of ISO-induced myocardial injury. SO(2) protects against ISO-induced PD173074 molecular weight myocardial injury associated with increased myocardial antioxidant capacity in rats. Laboratory Investigation (2011) 91, 12-23; doi:10.1038/labinvest.2010.156; published online 23 August 2010″
“Amyloid beta (A beta) deposition in the brain is considered the initiating event in the progression of Alzheimer’s disease (AD). Amyloid imaging is widely studied in diagnosing AD and evaluating the disease stage, with considerable advances achieved in recent years. We have developed a novel F-19-containing curcumin derivative (named FMeC1) as a potential imaging agent. This compound can exist in equilibrium between keto and enol tautomers, Cepharanthine with the enol form able to bind A beta aggregates while the keto form cannot. This study investigated whether FMeC1 is suitable as
a F-19 magnetic resonance imaging (MRI) probe to detect A beta deposition in the Tg2576 mouse, a model of AD. In F-19 nuclear magnetic resonance (NMR) spectra obtained from the whole head, a delayed decreased rate of F-19 signal was observed in Tg2576 mice that were peripherally injected with FMeC1 in comparison to wild-type mice. Furthermore, F-19 MRI displayed remarkable levels of F-19 signal in the brain of Tg2576 mice after the injection of FMeC1. Histological analysis of FMeC1-injected mouse brain showed penetration of the compound across the blood brain barrier and binding to A beta plaques in peripherally injected Tg2576 mice. Moreover, the distribution of A beta deposits in Tg2576 mice was in accordance with the region of the brain in which the F-19 signal was imaged. FMeC1 also exhibited an affinity for senile plaques in human brain sections.