Why the study?
Does codelivery of doxorubicin and sodium tanshinone IIA sulfonate using multicompartmentalized vesosomes enhance synergism and prevent doxorubicin-induced cardiomyocyte apoptosis in vitro?
Does codelivery of doxorubicin and sodium tanshinone IIA sulfonate using multicompartmentalized vesosomes enhance synergism and prevent doxorubicin-induced cardiomyocyte apoptosis in vitro?
Codelivery of doxorubicin and sodium tanshinone IIA sulfonate via multicompartmentalized vesosomes may offer a strategy to maintain antitumor efficacy while reducing doxorubicin-induced cardiotoxicity.
May support vesosome codelivery to limit doxorubicin cardiotoxicity; leaves open in vivo validation before clinical consideration.
Doxorubicin, one of the most effective antitumor drugs, causes serious adverse cardiac effects. As a derivative of tanshinone IIA, sodium tanshinone IIA sulfonate was exploited for curing cardiovascular disorders. The synergistic effect of the above drugs as a combination was investigated for treating cancer cells and attenuating myocardial apoptosis. A multicompartmentalized vesosome (MCV) was produced to co-deliver the drug combination. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and western blotting analysis demonstrated that the MCV can enhance the synergistic effect of the drug combination and promote the protection of STS in Dox-induced cardiomyocyte apoptosis.
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Zhang et al. (2018) studied this question.
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