Berberine Ameliorates Methionine-Induced Hyperhomocysteinemia and Biochemical Alterations in Male Rats
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Hyperhomocysteinemia, characterized by elevated plasma homocysteine levels, is associated with oxidative stress and metabolic dysfunction. This study evaluated the protective effects of berberine, a natural alkaloid compound, against methionine-induced biochemical alterations in male rats. Thirty-two adult male albino rats were randomly divided into four groups (n=8 each) and treated orally for eight weeks: Group 1 (negative control) received standard diet and water; Group 2 (positive control) received methionine (100 mg/kg); Group 3 received methionine (100 mg/kg) plus berberine (40 mg/kg); and Group 4 received berberine (40 mg/kg) alone. Serum samples were analyzed for homocysteine (Hcy), electrolytes (sodium, potassium, chloride), and creatine phosphokinase (CPK) enzyme activity. Methionine treatment significantly elevated homocysteine and CPK levels while reducing sodium and chloride concentrations compared to controls. Co-administration of berberine with methionine markedly decreased homocysteine levels from 76.5 to 12.2 micromole/L and normalized CPK activity. Berberine also restored sodium and chloride concentrations to near-normal levels. The berberine-only group exhibited biochemical parameters comparable to the negative control, confirming its safety profile. These findings demonstrate that berberine effectively mitigates methionine-induced biochemical disturbances through multiple mechanisms, including antioxidant effects, activation of the AMPK pathway, and reduction of reactive oxygen species. Berberine also protected electrolyte homeostasis and mitochondrial function. Therefore, berberine represents a promising natural therapeutic agent for preventing oxidative stress and metabolic complications associated with hyperhomocysteinemia, with potential applications in clinical management of homocysteine-related disorders.
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