الفهرس 
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Abstract
The current work was designed to detect the possible potential hepatoprotective effect of the aquatic blue green alga Aphanizomenon flos-aquae (AFA) and the therapeutic effect of both of AFA and silymarin against hepatic intoxication induced by carbon tetrachloride (CCl₄) in adult male mice. A total of 56 Swiss adult albino mice (Mus musculus) of CD1 strain, were allotted to eight groups, each group of seven mice. group (Ⅰ) negative control group: contains normal healthy mice; group (Ⅱ) positive control group: they are mice who received a dose of CCl₄ (0.5 mg/kg), dissolved in olive oil, through intraperitoneal injection twice-a-week for six weeks; group (Ⅲ) olive oil group: The mice received a daily oral dose of olive oil (0.1 mg/kg) (the vehicle); group (Ⅳ) AFA control group: received a daily oral dose of AFA (72.8 mg/kg) for 10 consecutive days; group (Ⅴ) silymarin control group: received a daily oral dose of silymarin (36.4 mg/kg) for 10 consecutive days; group (Ⅵ) AFA prophylactic group: they are mice that were given a daily oral prophylactic dose of AFA (72.8 mg/kg) for a period of 10 consecutive days prior to treatment with CCl₄; group (Ⅶ) AFA therapeutic group: they are mice who received a dose of CCl₄ (0.5 mg/kg), dissolved in olive oil, through intraperitoneal injection twice-a-week for six weeks, then received a daily oral therapeutic dose of AFA (72.8 mg/kg) for 10 consecutive days; group (Ⅷ) silymarin therapeutic group: they are mice who received a dose of CCl₄ (0.5 mg/kg), dissolved in olive oil, through intraperitoneal injection twice-a-week for six weeks, then mice received a daily oral therapeutic dose of silymarin (36.4 mg/kg) for 10 consecutive days.
Carbon tetrachloride caused liver damage as shown by biochemical results as there was marked increase in serum liver enzymes (AST and ALT) and MDA level in the hepatic tissue. As well, a remarkable decrease in anti-oxidant enzymes such as: SOD and CAT was noticed. On the other hand, protection offered by Aphanizomenon flos-aquae showed obvious decrease in AST, ALT and MDA levels, and increase in levels of SOD and CAT. Also, both AFA and silymarin showed therapeutic effect against the damage caused by CCl₄ as the levels of AST, ALT and MDA showed significant decrease, and the levels of SOD and CAT showed notable increase.
Carbon tetrachloride also caused liver damage as evidenced by marked changes in the hepatic architecture such as hemolysed blood in the branches of hepatic portal vein, venous congestion, and infiltration with inflammatory cells. The hepatocytes suffered from perinuclear halo,
presence of some multinucleated giant cells and necrosis. A severe extent of fibrosis was observed, associated with marked disruption in distribution of reticulin fibres. An excessive deposition of reticulin in the Glisson’s capsules was observed. Also, abnormal pattern of distribution of collagen fibres and excessive deposition of collagen around portal area and the Glisson’s capsule were observed. As well, extension of collagen fibres formed fibrous septa. Nodules were observed ”a sign of cirrhosis”. In the semithin sections severe damages were observed such as the excessive fatty degeneration, and accumulation of fat droplets together with presence of karyolysed, and karyorrihxed nuclei. However, protection by AFA and treatment with AFA therapeutic dose and silymarin therapeutic dose suppressed significantly liver damage induced by CCl₄; as the hepatic architecture of specimens from livers of mice from these groups showed almost no change compared with the negative control group. Just mild pathological features were observed such as mild vacuolization of cytoplasm due to hydropic degeneration, hyperplasia of bile ducts and presence of some inflammatory infiltrates around portal area. As well, the reticulin distribution was normal. Mild accumulation of collagen around portal area and central veins was observed.
At the ultrastructural level marked changes in the normal cellular structure of the hepatocytes were caused by CCl₄ such as swelling of mitochondria, loss of glycogen rosettes, condensation of chromatin, and loss of definitive shape of the nucleus. Each of AFA prophylactic group, AFA therapeutic group, and silymarin therapeutic group suppressed significantly cellular damage caused by CCl₄; as indicated by normal nucleus and nuclear chromatin distribution, increase in glycogen content, and normal mitochondrial