Bombax ceiba flowers extract ameliorates hepatosteatosis induced by ethanol and relatively moderate fat diet in rats.

Chronic excessive alcohol consumption could induce serious liver injury. In this study, therapeutic effect of aqueous methanol extract of Bombax ceiba L. flowers (BCE) (Family: Bombacaceae) was investigated against hepatic steatosis. This study included seven groups, and the research period was eight weeks. The first group served as control. The six remaining groups were divided into two categories, three groups in each. The first category was fed fat diet. The second category was fed fat diet and orally administrated ethanol, which was given in graduate doses from 2 g/kg/d to 6 g/kg/d. Then, one group from each category was orally treated with the standard drug fluvastatin (2 mg/Kg/d). Another group was orally treated with BCE (200 mg/kg/d). The third group left untreated. The results revealed that BCE significantly decrease both the body and liver weight. The treatment with BCE extract also ameliorates the effect of alcohol induced increase of liver enzyme activities. In addition, the extract was significantly increased hepatic liver antioxidants and decreased malondialdehyde (MDA) level. Also, serum lipid profiles: triglycerides (TG), total cholesterol (TC) and low density lipoprotein (LDL) were significantly decreased after BCE treatment. Histopathological study showed fatty changes induced by alcohol which were improved by BCE treatment. These data suggest that the BCE has anti-inflammatory, anti-oxidant and anti-steatosis potential properties against alcohol induced liver damage. This may be due to the presence of flavonoids and other phenol compounds.

The effect of antidepressant drugs on thioacetamide-induced oxidative stress.

OBJECTIVE: The aim of the present study was to investigate the effect of the serotonin selective reuptake inhibitors (SSRIs) fluoxetine and sertraline and the tricyclic drug imipramine on oxidative stress in the brain and liver caused by thioacetamide in rats. MATERIALS AND METHODS: Drugs were administered orally once daily at doses of 10 and 20 mg/kg for two weeks prior to intraperitoneal injection of thioacetamide (300 mg/kg). Rats were euthanized 24 h after thioacetamide. Reduced glutathione (GSH), malondialdehyde (MDA) and nitric oxide were measured in brain and liver. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) were measured in serum and histopathological evaluation of liver injury was performed. RESULTS: The administration of thioacetamide increased MDA by 151.8% and 161.2%, increased nitric oxide by 57.2% and 63.9% and decreased GSH by -40.6% and -67% in the brain and liver, respectively. Thioacetamide markedly increased serum ALT, AST and ALP by 277.8, 80.8 and 121%, respectively. In the brain, MDA was decreased in rats treated with fluoxetine or sertraline. The level of GSH increased by fluoxetine and by the higher dose of sertraline. Nitric oxide in brain was unchanged by fluoxetine, but increased after sertraline at 20 mg/kg. Brain MDA was increased by imipramine, which also decreased brain nitrite level. In the liver, fluoxetine or sertraline treatment increased GSH and nitrite levels. MDA was also increased by either drug. The drugs markedly decreased ALT, but increased ALP in serum. Meanwhile, imipramine decreased liver nitric oxide levels (at the lower dose only -32.9%), markedly increased hepatic GSH, but did not change MDA level. Serum ALT decreased by imipramine (but AST and ALP showed no change). Histopathological and histochemical examinations indicated that thioacetamide-induced liver injury was not decreased after treatment with the antidepressant drugs. CONCLUSIONS: In thioacetamide-treated rats, pretreatment with the SSRIs drugs fluoxetine and sertraline is associated with decreased lipid peroxidation in brain; liver peroxidation, however, is increased. Imipramine displayed opposite effects. The thioacetamide-induced hepatic damage was not reduced by fluoxetine, sertraline or imipramine.  

The protective effects of fish oil and artichoke on hepatocellular carcinoma in rats.

BACKGROUND AND OBJECTIVES: The present study aimed to evaluate the effect of fish oil and Artichoke (Cynara scolymus I.) against diethylnitrosamine (DEN) induced hepatocellular carcinoma in rats. MATERIALS AND METHODS: Animals were divided into 8 groups. Group 1, control rats. Group 2: rats injected with single dose of DEN (100 mg/kg body weight). Groups 3-8 supplemented with different concentrations of either fish oil or artichoke for 25 days before DEN injection. RESULTS: DEN treatment revealed a significant decrease in tissue xanthine oxidase (XO), glutathione, glutathione-s-transferase (GST), and a marked increase in malondialdehyde (MDA) and nitric oxide (NO) levels. Vascular endothelial growth factor (VEGF), alpha-fetoprotein (AFP), and ferritin levels showed a significant increase. A significant increase in serum aspartate amino transferase (AST), alanine amino transferase (ALT), gamma glutamyl transferase (GGT), alkaline phosphatase (ALP), and total bilirubin levels were found. A significant decrease in tissue total proteins and serum albumin was observed. The administration of DEN affected the liver cell through occurrence of hepatic cellular degeneration and necrosis. Treatment with fish oil (5%, 10%) or artichoke heads or leaves (0.5, 1 g) for 25 days led to significant amelioration of DEN-induced changes in the biochemical parameters. An almost normal histological architecture of the liver, in treated groups, was showed as compared to the controls. CONCLUSIONS: The results pointed that 10% fish oil and 1 g% leaves of artichoke succeeded to protect from hepatocellular carcinoma to a certain degree. In addition, they may be considered as protective foods against angiogenesis.