الفهرس 
REVIEW OF LITERATUREOnly 14 pages are availabe for public view
 |  | from | 253 |  |  |
| | | from | 253 | | |
Abstract
Phytochemical and nutroutical researches have suggested that flavonoids exhibit a pharmacological, therapeutic and chemo protective properties. Specifically some earlier studies have shown that, total flavonoids and polyphenolic compounds of cinnamon extract provide excellent protection against toxicities induced by xenobiotics, such as nitrosamine. This study, antioxidant and hepatoprotective effects of total flavonoids & phenolcs from ethanolic cinnamon flavonoid extract (CFE) against toxicities of DBN were evaluated in vivo by measuring the biological, histopathological, biochemical changes in serum & liver tissue as well as DNA fragmentation in liver and spleen of 90 female rats, which were divided into 6 groups of 15 rats; normal control group, N-N-dibutylnitrosamine (DBN) model group, CFE 150mg/kg group, CFE 300mg/kg group, CFE 150mg/kg plus DBN group and CFE 300mg/kg plus DBN group. Results demonstrated that DBN caused a significant (p< 0.05) decrease in the total body weight, liver weight, GSH, SOD, total protein (serum & liver tissue) and albumin while kidney weight, spleen weight, ALT, AST, ALP, total bilirubin, G ratio, urea and creatinine increased all over the experiment period when compared with the control group. In vivo, oral treatment with CFE alone at doses 150 and 300mg/kg caused a significant (p< 0.05) increase in the total body weight, GSH, SOD, total protein (serum &liver tissue, albumin and globulin while MDA, ALT, AST, ALP, total bilirubin and G ratio decreased all over the experiment period when compared with the control group. In vivo, oral treatment with CFE at doses 150 and 300mg/kg DBN caused a significant (p< 0.05) increase in SOD, GSH and total protein (serum & liver tissue) while MDA, ALT, AST, ALP, total bilirubin, albumin and G ratio decreased all over the experiment period when compared with DBN model group. In DNA fragmentation test for liver and spleen, DBN induced apoptosis in liver and spleen. While both doses CFE acts as anti- apoptotic agent, this effect was detected in spleen more than the liver. Feeding with CFE and treatment with DBN also, induced little apoptosis in spleen and liver after 4 weeks but after 12 ,observable increase of apoptotic bands was recorded in liver and spleen. Histopathological examination of organs (liver, kidney and urinary bladder) correlated strongly with the biochemical changes and DNA fragmentation test where treatment with DBN alone had a toxic effect on liver through degeneration hyperemia, inflammatory reaction. And kidney through hemorrhages renal casts hyperemia, inflammatory reaction. And also urinary bladder through papillary hyperplasia with papillary projection formation in the cell layer of the lining epithelium. Feeding with CFE alone leading to hyperemia in the liver and kidney an short time then the organs back to normal an the long duration due to adaptation. Feeding with CFE plus DBN act as a protector against nitrosamine toxicity mainly on liver and urinary bladder and secondary on the kidney. The results indicate that CFE has strong antioxidant and hepatoprotective activity against toxicity of dibutylnitrosamine. To understand the exact components of CFE responsible for the hepatoprotective effect, eleven flavonoid & phenolic compounds were identified from CFE.
Keywords: Photochemical, phenolic compounds, flavonoids, dibutylnitrosamine, Cinnamon, MDA, GSH, SOD, ALT, AST, ALP, total bilirubin, total protein, albumin, Histology, DNA fragmentation.