The hypothesis was tested that vitamin E protects chickens from a lethal Escherichia coli infection by inhibiting the biosynthesis of prostaglandins, thereby activating humoral immunity and phagocytosis. When chickens were fed supplement vitamin E at the level of 300 mg/kg diet, which is six times the presently used dietary level, endogenous PGE1, PGE2, and PGF2 alpha levels decreased in the immunopoietic organs, bursa, and spleen. Antibody titers to E. coli lipopolysaccharide and phagocytosis increased at the same time. Infection slightly increased prostaglandin levels and vitamin E appeared to compensate for this increase. Aspirin, a known prostaglandin inhibitor acted synergistically with vitamin E in depressing endogenous PG levels in bursa and decreasing mortality from E. coli infection.

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BackgroundGmelina arborea (GA) is widely used in traditional medicine for treating a number of ailments including gastrointestinal tract disorders.ObjectiveTo evaluate the gastroprotective effect of GA stem bark against ethanol-induced gastric ulcer in Wistar rats.Materials and methodsAll animals were fasted for 36 h and received GA extract 250 and 500 mg/kg body weight (bw), 1 h before the administration of ethanol. The animals received ranitidine 50 mg/kg bw which served as the standard. The rats were sacrificed after 4 h. Then, the injuries to the gastric mucosa were estimated through gross evaluation of ulcer lesions and histology. The antioxidant parameters such as level of lipid peroxidation, superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GPx) in gastric tissue were also determined.ResultsGA treatment at a dose of 500 mg/kg bw offered 91.98% inhibition of ulcer formation, which is higher than that of ranitidine. The ethanol treatment extensively increased lipid peroxidation and it was significantly (P < 0.01) reduced in GA-treated group that eventually helped to prevent free radical accumulation. The GA enhanced the gastric mucosal antioxidant system, as indicated by a dose-dependent increase in the level/activities of GSH, GPx, and SOD. GA also attenuated the severity of histological signs of cell damage. Further, GA extract showed in-vitro 2,2-diphenyl-1-picrylhydrazyl radical scavenging activity with IC50 value of 124.39 μg/ml.ConclusionThe results indicate that the gastroprotective effect of GA is probably related to its antioxidant activities that protect gastric mucosa against oxidative damage and antilipid peroxidative activity that maintain membrane integrity.

Non-alcoholic steatohepatitis (NASH) is a progressive form of Non-alcoholic fatty liver disease (NAFLD), a chronic liver disease with a significant unmet clinical need. In this study, we examined the protective effects of Garcinia indica extract standardized to contain 20% w/w of Garcinol (GIE) and 95% Curcuminoids w/w from Curcuma longa (Curcuminoids) in a Stelic animal model (STAM) of NASH. The STAM mice developed steatosis, hepatocyte ballooning, and inflammation, which were significantly reduced by the combination of GIE and Curcuminoids, resulting in a lower NAFLD activity score. The treatment reduced fibrosis as observed by Sirius red staining, liver hydroxyproline content and mRnA levels of tGf-β and collagen in the liver. Immunostaining with alpha-smooth muscle actin (α SMA) revealed a significant reduction in hepatic stellate cells. Intriguingly, the combination regimen markedly decreased the mRNA levels of MCP1 and CRP and both mRNA and protein levels of TNF-α. NF-kB, reduced the hepatic and circulating FGF21 levels and altered the nonenzymatic (glutathione) and enzymatic antioxidant markers (Glutathione peroxidase, and superoxide dismutase). Our results suggest that the combination of GIE and Curcuminoids can reduce the severity of NASH by reducing steatosis, fibrosis, oxidative stress, and inflammation. The results suggest that the combinatorial regimen could be an effective supplement to prevent the progression of liver steatosis to inflammation and fibrosis in NASH. Nonalcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disorders 1,2. It includes the spectrum of liver disease, ranging from benign fatty liver to hepatocellular carcinoma. It is histologically further categorized into the nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH). NAFL, as the early-stage disease shows the presence of excessive fat in the liver (hepatic steatosis) with no evidence of hepatocellular injury, while NASH is characterized by the accumulation of fat accompanied by infiltration of inflammatory cells and cellular damage, which can progress to cirrhosis, liver failure, and liver cancer 3. NASH is the hepatic manifestation of metabolic disorder and is closely associated with type 2 diabetes, obesity, insulin resistance anda systemic inflammatory state 4-8. Consequently, NASH patients have a higher risk of cardiovascular events and neoplasia, resulting in a higher rate of mortality 9,10. It is usually a silent disease with minimum symptoms, while weight loss, fatigue, and weakness develop as the disease progresses. Although the disease development and progression are still not well elucidated, the most accepted theory to explain the pathogenesis is "multiple-hits hypothesis". The initial hit leads to the development of simple steatosis, while liver cell inflammation and apoptosis are induced by secondary hits, leading to mitochondrial dysfunction, oxidative stress, lipid peroxidation, gut dysbiosis, and Kupffer cell activation, which finally results in NASH 11,12. Presence...

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