morin and Hepatic-Encephalopathy

This study aimed to investigate the possible usefulness of morin flavonoid in comparison to silymarin as a hepatic/neuronal-supportive agent with similar effects and higher bioavailability in a rat model of hepatic encephalopathy (HE). Morin effects on rat liver and brain were evaluated post-induction of HE by thioacetamide (TAA; 200 mg/kg/day for 3 successive days). Then, the serum activities of aspartate transaminase (AST) and alanine transaminase (ALT) together with ammonia concentration were estimated to assess the liver function. Also, the degree of brain effects was evaluated via the assessment of brain contents of reduced glutathione (GSH), malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin (IL-1β) together with glutathione peroxidase (GPx) activity. In addition, the apoptotic and inflammatory changes in brain and liver tissues were also assessed via immunohistochemical examination. Our findings revealed a promising effect of morin against HE complications; as it corrected the liver functions, attenuated the brain/liver tissue injuries, and reduced the apoptotic and inflammatory insults of HE on both organs. These effects are comparable to those of silymarin. Morin could be introduced as a promising hepato- and neuro-therapeutic adjuvant in HE-associated neuronal complications especially in cases like silymarin intolerance.

Topics: Alanine Transaminase; Ammonia; Animals; Antioxidants; Aspartate Aminotransferases; Flavones; Flavonoids; Glutathione; Glutathione Peroxidase; Hepatic Encephalopathy; Liver; Malondialdehyde; Oxidative Stress; Rats; Rats, Wistar; Silymarin; Thioacetamide; Tumor Necrosis Factor-alpha

Hyperammonaemia is a major contributing factor to neurological abnormalities observed in hepatic encephalopathy and in congenital defects of ammonia detoxication. Ammonia toxicity results in free radical generation that leads to oxidative stress and tissue damage. Morin is a bioflavonoid, a constituent of many herbs and fruits that are used as herbal medicines and also several biological activities. Our aim was to investigate the effect of morin on circulatory liver markers, lipid peroxidation and antioxidant status in ammonium chloride (AC)-induced hyperammonaemic rats.. Male albino Wistar rats weighing 180-200 g were used for the study. The hyperammonaemia was induced by interaperitonial injection of AC (100 mg/kg body weight). Rats were treated with morin (30 mg/kg body weight) via oral administration. Administration of morin in hyperammonaemic rats reduced the levels of ammonia and urea. The antioxidant property of morin was studied by assessing the activities of thiobarbituric acid reactive substances (TBARS), hydroperoxides (HP) and liver markers (alanine transaminase, aspartate transaminase and alkaline phosphatase) and the levels of glutathione peroxidase, superoxide dismutase, catalase, reduced glutathione, vitamins A, C and E in AC-treated rats.. Oxidative stress was effectively modulated by morin administration. Morin significantly improved the status of antioxidants and decreased the levels of ammonia, urea, TBARS, HP and liver markers enzymes, as compared to the AC-treated group.. The study offers evidence for the antihyperammonaemic, hepatoprotective and antioxidant effects of morin against oxidative stress induced by AC.

Topics: Ammonium Chloride; Animals; Antioxidants; Flavonoids; Free Radicals; Hepatic Encephalopathy; Hyperammonemia; Indicators and Reagents; Lipid Peroxidation; Liver; Male; Oxidation-Reduction; Rats; Rats, Wistar