Key result
Silymarin reverses arsenic-induced cardiotoxicity by reducing CK-MB and inflammation in rats.
Why the study?
Sodium arsenite poses substantial cardiovascular hazards via contaminated drinking water, and this study evaluated the cardioprotective role of the antioxidant and anti-inflammatory flavonolignan complex silymarin against subacute sodium arsenite-induced cardiovascular toxicity.
Does oral silymarin ameliorate subacute sodium arsenite-induced myocardial toxicity, oxidative stress, and inflammation in male Wistar rats?
Does oral silymarin ameliorate subacute sodium arsenite-induced myocardial toxicity, oxidative stress, and inflammation in male Wistar rats?
Answers are grounded in this paper and cite their sources.
In a preclinical rat model, oral silymarin demonstrated cardioprotective effects against sodium arsenite-induced myocardial toxicity by attenuating oxidative stress, TNF-α-mediated inflammation, and structural cardiac damage.
Sodium (meta) Arsenite (SA), a widely encountered environmental metalloid, poses substantial cardiovascular hazards, especially in regions affected by contaminated drinking water. Silymarin (SM), a flavonolignan complex known for its antioxidant, anti-inflammatory, and cytoprotective actions, has gained attention for its potential to counter chemical- induced tissue damage. The present study investigated the cardioprotective role of SM against subacute SA-induced cardiovascular toxicity in male Wistar rats. Twenty-four rats were randomly assigned into four groups (n = 6) : Control, SM alone (100 mg/kg administered orally from day 14), SA alone (10 mg/kg in drinking water for 28 days), and SA + SM. Physiological parameters, body weight, feed and water intake were routinely monitored. On day 29, animals were euthanized and samples were collected for biochemical, and histopathological evaluations. SA exposure caused reduced water intake, feed intake, and poor body weight gain. Hematological analysis showed that SA reduced RBC count, hemoglobin, and platelets and increased CK-MB. SA markedly elevated superoxide anion, lipid peroxidation, depleted GSH, and reduced antioxidant enzyme activities. TNF-α levels and cardiac mRNA expression were significantly up-regulated. Histopathology of the heart revealed hemorrhage, myocardial necrosis, fiber disintegration, and inflammatory cell infiltration.Treatment with SM improved physiological, hematological, and biochemical (CK-MB) parameters, restored antioxidant status, suppressed TNF-α levels and mRNA expression, and enhanced myocardial structural integrity. SA induced marked cardiotoxicity characterized by oxidative stress, inflammation, hematological alterations, elevated CK- MB, and myocardial structural damage. SM significantly reversed these changes by restoring antioxidant status, reducing TNF-α–mediated inflammation, and improving cardiac tissue integrity, demonstrating a protective effect against established arsenic-induced cardiotoxicity. These findings indicate that SM exhibits significant therapeutic potential in ameliorating established SA-induced cardiotoxicity, warranting further mechanistic and clinical investigation.
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Gurukiran et al. (2026) studied Sodium arsenite-induced myocardial toxicity (n=24). Silymarin vs. Sodium arsenite alone (10 mg/kg in drinking water for 28 days), Silymarin alone, and unexposed Control was evaluated on Biochemical (CK-MB, oxidative stress markers, TNF-α), hematological, physiological, and myocardial histopathological parameters at day 29. Silymarin (100 mg/kg) significantly reversed sodium arsenite-induced cardiotoxicity (10 mg/kg) in rats (n=24) by reducing CK-MB and TNF-α, restoring antioxidants, and improving myocardial structure.
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