Key result
Magnesium isoglycyrrhizinate dose-dependently ameliorated doxorubicin-induced acute cardiac and hepatic toxicity in mice by inhibiting oxidative stress and apoptosis.
Why the study?
Does magnesium isoglycyrrhizinate prevent doxorubicin-induced acute cardiac and hepatic toxicity in mice?
Does magnesium isoglycyrrhizinate prevent doxorubicin-induced acute cardiac and hepatic toxicity in mice?
p-value: p=<0.01
Magnesium isoglycyrrhizinate ameliorates doxorubicin-induced acute cardiac and hepatic toxicity in mice through anti-oxidant and anti-apoptotic mechanisms.
The present study investigated the effects and potential mechanisms of action of magnesium isoglycyrrhizinate (MgIG) in doxorubicin (DOX)-treated mice. Histopathological analysis and western blot analysis were conducted in the liver and heart tissues and biochemical analysis of the serum was performed. The results revealed that MgIG (10, 20 and 40 mg/kg/day) could protect the structure and functions of the liver and heart by inhibiting the activities of the myocardial enzymes creatine kinase (CK), CK-MB and lactate dehydrogenase and the hepatic-specific enzymes aspirate aminotransferase and alanine aminotransferase, increasing the activities of the antioxidants superoxide dismutase and glutathione peroxidase, and inhibiting cellular apoptosis induced by DOX (30 mg/kg). These results demonstrate that inhibiting lipid peroxidation and reducing myocardial and hepatocyte apoptosis may be one of the mechanisms by which MgIG exhibits hepatoprotective and cardioprotective effects in DOX-treated mice.
No takes yet. Share an insight, caveat, or question.
Wu et al. (2017) studied Doxorubicin-induced acute cardiac and hepatic toxicity (n=50). Magnesium isoglycyrrhizinate vs. Doxorubicin alone (30 mg/kg) and saline control was evaluated on Hepatic and cardiac injury markers (AST, ALT, CK, CK-MB, LDH) and apoptosis (p=<0.01). Magnesium isoglycyrrhizinate dose-dependently ameliorated doxorubicin-induced acute cardiac and hepatic toxicity in mice by inhibiting oxidative stress and apoptosis.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: