Time filter

Source Type

Chien K.-J.,Veteran General Hospital Kaohsiung | Chien K.-J.,Tajen University | Horng C.-T.,Tajen University | Horng C.-T.,Kaohsiung Armed Force General Hospital | And 4 more authors.
Life Science Journal | Year: 2013

Meloxicam (MXM) is a relatively new and a COX-2 preferential NSAID used for inflammation relief of sport injury with less gastrointestinal side effects such as peptic ulcers. The present study is to investigate the influence of running exercise training on pharmacokinetics of MXM in rats. In this study, animals (male SD rats) were divided into three groups: (1) sedentary group, (2) 4 weeks exercise group and (3) 8 weeks exercise group. Progressive training was adopted on a rodent treadmill machine. After single dose administration of MXM, blood samples were taken at different time points. Plasma was subjected to liquid-liquid extraction and further analyzed by a high-performance liquid chromatography (HPLC) method. Chromatographic separation was performed on a Cosmosil 5C18-AR-II reverse-phase HPLC column (150 × 4.6mm i.d., 5 μm) with a mobile phase of 20mM potassium dihydrogen phosphate-acetonitrile (60:40, v/v, pH 3.5) and UV detection at a wavelength of 355 nm. The CYP2C9 is one of most important enzyme affecting the metabolism of non-steroidal anti-inflammatory drugs in the liver. This study also determined CYP2C9 activity to explore the running exercise training on the correlation of liver enzymes and blood levels of MXM. The results revealed that long term running exercise can increase Tmax and decrease Cmax and the area under curve (AUC), which could be associated with the liver microsomal CYP2C9 activity.

Wang M.-E.,National Taiwan University of Science and Technology | Chen Y.-C.,National Taiwan University of Science and Technology | Chen I.-S.,Veteran General Hospital Kaohsiung | Hsieh S.-C.,National Taiwan University of Science and Technology | And 2 more authors.
Journal of Nutritional Biochemistry | Year: 2012

Inflammation and hepatic stellate cell (HSC) activation are the most crucial steps in the formation of hepatic fibrosis. Hepatocytes damaged by viral or bacterial infection, alcohol or toxic chemicals initiate an inflammatory response that activates collagen production by HSCs. Recent studies indicate curcumin has liver-protective effects due to its anti-inflammatory, antioxidant and anticancer activities; however, the mechanisms are not well understood. In this study, we show that curcumin protected against hepatic fibrosis in BALB/c mice in vivo by inhibiting HSC activation, inflammatory responses and inducing apoptosis of damaged hepatocytes. Using the thioacetamide (TAA)-induced hepatic fibrosis animal model, we found that curcumin treatment up-regulated P53 protein expression and Bax messenger RNA (mRNA) expression and down-regulated Bcl-2 mRNA expression. Together, these responses increased hepatocyte sensitivity to TAA-induced cytotoxicity and forced the damaged cells to undergo apoptosis. Enhancing the tendency of damaged hepatocytes to undergo apoptosis may be the protective mechanism whereby curcumin suppresses inflammatory responses and hepatic fibrogenesis. These results provide a novel insight into the cause of hepatic fibrosis and the cytoprotective effects curcumin has on hepatic fibrosis suppression. © 2012.

Loading Veteran General Hospital Kaohsiung collaborators
Loading Veteran General Hospital Kaohsiung collaborators