protective effect of some polyphenolic compounds on lipopolysaccharide-induced hepatitis in D-galactosamine sensitized rats

To study the hepatoprotective effect of teas and cocoa extracts against liver injury and to know the potent effect of each in protecting the liver from Lipopolysaccharide-induced hepatitis in D-galactosamine sensitized rats. Rats were divided into eight groups; group I received saline, groups II, III and IV received black tea, green tea and cocoa extracts respectively orally for one month; group V received saline, groups VI, VII and VIII received black tea, green tea and cocoa extracts respectively orally for one month before induction of hepatitis. Indicated that the prophylactic study significantly improved serum hepatic enzymes; liver oxidants/antioxidants profile and serum tumor necrosis factor-a levels compared to DGa1N / LPS group. Green tea extract showed the maximum improvement in liver enzymes and oxidants/antioxidants profile in prophylactic groups. Also cocoa extract showed the maximum improvement in tumor necrosis factor-a levels compared to green and black tea prophylactic groups. The antihepatotoxic effect of teas and cocoa was attributed to their free radical scavenging antioxidants [catechins, epicatechins and procyanidins] which protected the liver from oxidative damage

Obesity increases transcription of heme oxygenase-1 gene and synergistically stimulates angiogenesis with vascular endothelial growth factor and plasminogen activator inhibitor-1 in rats

Angiogenesis plays an important role in obesity; heme oxygenase-1 [HO-1] has been implicated in the process of angiogenesis. To investigate the effect of obesity on transcription of HO-1 gene and to study the relation between elevated HO-1 and other angiogenic factors such as vascular endothelial growth factor [VEGF] and plasminogen activator inhibitor -1 [PAI-1] which are though to play an important role in the pathogenesis of obesity. Obesity was induced in 15 albino rats by feeding high fat diet for 3 months to establish diet-induced obesity. Another 15 rats were used as control. Blood samples were collected from tail vein; plasma PAI-1, lipid profile, free fatty acids [FFA], leptin and VEGF were measured. RNA was extracted from liver of obese and normal rats and RT-PCR was done, beta-actin mRNA expression for each sample was used as internal control. In rats fed high fat diets for 3 months, the total body weight were significantly increased [247.0 +/- 14.66g] compared to control group [126.37 +/- 23.26 g]. Obese rats showed a significant increase in serum triacylglycerol [TAC], total cholesterol [TC], low density lipoproteins-cholesterol [LDL-C], leptin and plasma free fatty acids, while serum high-density lipoproteins-cholesterol [HDL-C] was significantly decreased. HO-1-mRNA was increased in liver homogenates of obese rats compared to non-obese rats. These results indicate that the body response to obesity by elevating the expression of the stress gene HO-I. Angiogenic factors VEGF and PAI-I were significantly increased in obese compared to non-obese rats. Our findings suggest that HO-I and angiogenic factors [VEGF and PAI-I] play an important role in pathogenesis of obesity