Key result
Rheum turkestanicum extract improves viability and reduces apoptosis in doxorubicin-treated cardiomyocytes.
Why the study?
Does Rheum turkestanicum extract prevent doxorubicin-induced toxicity in H9c2 cells?
Does Rheum turkestanicum extract prevent doxorubicin-induced toxicity in H9c2 cells?
Rheum turkestanicum extract exerts cardioprotective effects against doxorubicin-induced toxicity in H9c2 cells by reducing oxidative stress and apoptosis.
Supports further preclinical testing of herbal extracts against anthracycline toxicity; leaves open in vivo and clinical translation.
Doxorubicin is a chemotherapy drug but its clinical using is limited because of its cardiotoxicity. Reactive oxygen species play an important role in the pathological process. The aim of this study is to evaluate the protective effect of Rheum turkestanicum Janisch., Polygonaceae, against doxorubicin-induced apoptosis and death in H9c2 cells. The cells were incubated with different concentrations of R. turkestanicum extract and N -acetylcysteine as positive control for 2 h, followed by incubation with 5 μM doxorubicin for 24 h. Cell viability and apoptotic induction were determined by using MTT and PI assays, respectively. The level of reactive oxygen species and lipid peroxidation was measured by fluorimetric methods. Doxorubicin significantly decreased cell viability which was accompanied by an increase in ROS production and lipid peroxidation. Pretreatment with R. turkestanicum increased the viability of cardiomyocytes and could decrease lipid peroxidation and reactive oxygen species generation. Also, R. turkestanicum attenuated apoptotic induction. N -acetylcysteine at 100 μM reduced the levels of reactive oxygen species and lipid peroxidation. But, treating H9c2 cells with N -acetylcysteine did little to protect H9c2 cells from doxorubicin-induced cell death. R. turkestanicum exerts protective effect against oxidative stress-induced cardiomyocytes damage. Our findings showed that R. turkestanicum could exert the cardioprotective effects against doxorubicin-induced toxicity partly by anti-apoptotic activity. Also, N -acetylcysteine prevented oxidative stress via reduction of reactive oxygen species and lipid peroxidation. N -acetylcysteine induced less protective effects than R. turkestanicum extract against doxorubicin-induced cytotoxicity.
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Hosseini et al. (2016) studied Doxorubicin-induced cardiotoxicity. Rheum turkestanicum extract vs. Doxorubicin alone and N-acetylcysteine was evaluated on Cell viability and apoptotic induction. Rheum turkestanicum extract increased viability and decreased lipid peroxidation, reactive oxygen species, and apoptosis in doxorubicin-treated H9c2 cardiomyocytes.
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