RESUMEN
In Taiwan, Corchorus capsularis L. has long been cultivated and the leaves are consumed as edible vegetable. This study is to investigate the protection effect of extract of C. capsularis leaves (ECC) on ethanol-induced acute gastric mucosal lesion (AGML) in rats. The results of phytochemical determination in ECC for total polyphenol, flavonoid and polysaccharide were 59.88 ± 0.61 mg/g, 86.39 ± 18.0 mg/g and 320.89 ± 6.99 mg/g, respectively. ECC showed significant activity of 1,1-diphenyl-2-picrylhydrazyl (DPPH) free radical scavenging with IC50 of 0.25 mg/ml. In vivo studies, Sprague-Dawley (SD) rats were randomly divided into five groups: sham, vehicle (control) and low-, medium-, and high-dose ECC (LECC, MECC, HECC; 200, 400, and 1,000 mg/kg/day, respectively). ECC was able to decrease significantly the ulcer index (UI) caused by 80% ethanol in a dose dependent manner. There was no significant effect on growth trend and food intake rate after the administration of ECC in the experimental period. The serum lipid parameters in ECC groups revealed significant increase in glutathione peroxidase (GPx), superoxide dilmutase (SOD) and catalase (CAT), and a decrease in malondialdehyde (MDA). Significant amelioration on pathological lesion score was found in ECC groups compared with the control group (P<0.05). The overall results indicate that ECC has protective effects on ethanol-induced AGML in rats, which could be associated with its antioxidant activity.
Asunto(s)
Corchorus/química , Extractos Vegetales/farmacología , Úlcera Gástrica/tratamiento farmacológico , Animales , Relación Dosis-Respuesta a Droga , Etanol/efectos adversos , Hojas de la Planta/química , Ratas Sprague-Dawley , Úlcera Gástrica/inducido químicamenteRESUMEN
Exposure to particulate matter (PM) increases the incidence of cardiovascular disease, but the underlying mechanisms remain unclear. To characterise ambient PM collected from a coach station in an urban area, particulate polycyclic aromatic hydrocarbons (PAHs) and trace metals were evaluated, and diagnostic ratios were then used to determine the sources based on the PAHs identified in PM. To elucidate the mechanism of PM-induced vascular toxicology, human coronary artery endothelial cells (HCAECs) were exposed to PM, PM-free supernatant and residual PM, and the associations between PAHs and trace metals, nitric oxide (NO), endothelin-1 (ET-1) and interleukin-6 (IL-6) were investigated. Petrogenic-related particulate emissions, such as vehicle exhaust, accounted for 68.75% and 75.00% of mass in the 0.1-1-µm PM (PM(0.1-1)) and <0.1-µm PM (PM(0.1)) size fractions, respectively. Vehicle exhaust particles (VEPs) caused significant NO suppression and increase in ET-1 and IL-6, whereas residual PM caused an increase in NO, ET-1 and IL-6 compared with the effects of the corresponding supernatants. PAHs in PM, particularly those with 4-6 rings, were associated with NO suppression, and ET-1 and IL-6 were positively correlated with the amount of trace metal compounds. These findings suggest that chemical components affect the regulation of vasoactive function and inflammation.