Key result
Pre-treatment with deep sea water of 1,500 hardness significantly increased the viability of doxorubicin-treated H9c2 cardiomyocytes from approximately 60% to over 90% at 48 hours.
Why the study?
Does deep sea water pre-treatment prevent doxorubicin-induced cardiotoxicity in rat H9c2 cardiac muscle cells?
Does deep sea water pre-treatment prevent doxorubicin-induced cardiotoxicity in rat H9c2 cardiac muscle cells?
Absolute Event Rate: 90% vs 60%
p-value: p=<0.001
Deep sea water protects against doxorubicin-induced cardiotoxicity in vitro by inhibiting DNA damage and apoptosis, suggesting potential as a protective supplement during chemotherapy.
Deep sea water pre-treatment may protect cardiomyocytes from doxorubicin in vitro; leaves open any clinical role and requires human trials.
Doxorubicin (DOX) is one of the most effective chemotherapeutic agents in the treatment of a variety of tumors. However, its clinical use has been compromised by the risk of cardiotoxicity. Thus, many efforts have been focused on exploring new strategies to prevent or reverse DOX-induced cardiotoxicity. Recently, deep sea water (DSW) has drawn much scientific interest for therapeutic intervention due to its enrichment in nutrients and minerals. In this study, we investigated whether DSW has protective effects against DOX-induced cardiotoxicity. Pre-treatment with DSW significantly increased the viability of DOX-treated rat H9c2 cardiac muscle cells. This protective effect of DSW appears to be mediated through the inhibition of DNA damage rather than suppression of reactive oxygen species (ROS) production in DOX‑treated H9c2 cardiac muscle cells. The inhibitory effect of DSW on DOX-induced DNA damage subsequently attenuated apoptotic signaling such as activation of cysteine-aspartic acid protease-3 (caspase-3) and fragmentation of poly(ADP-ribose) polymerase (PARP), whereas the expression of anti-apoptotic protein B-cell lymphoma-extra large (Bcl-xL) was increased. Moreover, DSW treatment rescued the activation of protein kinase B (Akt) to protect cells from DOX-triggered apoptosis. Taken together, our data showed that DSW has protective effects against DOX-induced cardiotoxicity, suggesting that DSW has some promise as a novel protective supplement for promoting the successful use of DOX in clinical regimen.
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Lee et al. (2014) studied Doxorubicin-induced cardiotoxicity. Deep sea water (DSW) vs. Doxorubicin alone was evaluated on Cell viability (p=<0.001). Pre-treatment with deep sea water of 1,500 hardness significantly increased the viability of doxorubicin-treated H9c2 cardiomyocytes from approximately 60% to over 90% at 48 hours.
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