Silymarin attenuates cobalt chloride-induced redox imbalance and cardio-renal dysfunctions in rats

Silymarin is an extract of <i>Silybum marianum</i> that is used traditionally for the treatment of several diseases. This study sought to evaluate the protective effects of silymarin on cobalt chloride (CoCl₂)-induced cardio-renal toxicities in rats. Forty rats were randomly divided into four groups of 10 rats each: control; 300 mg/kg CoCl₂; CoCl₂ + 100 mg/kg silymarin; and 100 mg/kg silymarin only. All administrations were done orally. At the end of the experimental period (seven days), blood pressure parameters, markers of oxidative stress, antioxidant defense status, renal function test, histopathology and immunohistochemical expressions were evaluated on the heart and kidney tissues. Silymarin significantly (<i>p</i> < 0.05) altered CoCl₂-induced alterations in blood pressure parameters, antioxidants and markers of oxidative stress, blood urea nitrogen and creatinine. Histopathological evaluation revealed area of infiltration of the myocardium by inflammatory cells and hemorrhages in the kidney of rats exposed to CoCl₂ without silymarin treatment, but these lesions were absent in the control and silymarin groups. Increased immunohistochemical expression of cardiac troponin I and matrix metalloproteinase-2 (MMP-2) was observed in the cardiac tissues of rats exposed to CoCl₂ without silymarin treatment. The immunohistochemical expression of cystatin C was heightened, while that of angiotensin-converting enzyme 2 (ACE2) was attenuated in the CoCl₂ untreated group compared with the control and silymarin groups. In conclusion, silymarin effectively mitigated the toxic effects of CoCl₂ on the heart and kidney tissues of rats due to its ability to positively modulate the activities of endogenous antioxidants and neutralize reactive oxygen species in cardiac and renal systems.