Abstract Title

Screening the ability of BNS-22 against chemotherapy-induced cytotoxicity in Cardiomyocytes

Presenter Name

Dane Eskildsen

RAD Assignment Number

309

Abstract

Hypothesis:

Cardiac toxicity is one of the leading contraindications to many chemotherapeutic agents including anthracyclines (e.g. Doxorubicin). It has been demonstrated that knocking out the beta isozyme of topoisomerase II in mice results in amelioration of the cardiotoxic effects of Doxorubicin. The purpose of this study is to evaluate whether or not the inhibiton of the Topoisomerase II beta isozyme by the drug BNS-22 in cardiomyocytes can alleviate the cardiotoxic effects of doxorubicin.

Methods/Materials:

Cardiomyocyte cells (H9C2) were used to evaluate the cytotoxicity of BNS-22. Additionally, these cardiomyocytes were used to determine the rate of cardiac cell death in cells treated with Doxorubicin and BNS-22 concurrently compared to cells treated with Doxorubicin alone. Cell viability was measured by luminescence assay using the CellTiter-Glo kit. Cell viability was measured 72 hours after the administration of Vehicle (control) or BNS-22 or doxorubicin or doxorubicin and BNS-22.

Results:

Cardiomyocytes (H9C2) were grown following standard cell culture conditions. Cells which were treated with both Doxorubicin and BNS-22 together and the cells treated with only BNS-22 suffered considerably less cell loss than the cells treated with Doxorubicin alone.

Conclusions:

These preliminary results suggest that BNS-22 helps to alleviate the cardiotoxic effects of Doxorubicin. This experiment provides some evidence for the use of Topoisomerase inhibitors in the treatment of doxorubicin induced cardiotoxicity. Further cell viability assays using this drug will be performed to substantiate current findings.

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Research Area

Cancer

Presentation Type

Poster

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Screening the ability of BNS-22 against chemotherapy-induced cytotoxicity in Cardiomyocytes

Hypothesis:

Cardiac toxicity is one of the leading contraindications to many chemotherapeutic agents including anthracyclines (e.g. Doxorubicin). It has been demonstrated that knocking out the beta isozyme of topoisomerase II in mice results in amelioration of the cardiotoxic effects of Doxorubicin. The purpose of this study is to evaluate whether or not the inhibiton of the Topoisomerase II beta isozyme by the drug BNS-22 in cardiomyocytes can alleviate the cardiotoxic effects of doxorubicin.

Methods/Materials:

Cardiomyocyte cells (H9C2) were used to evaluate the cytotoxicity of BNS-22. Additionally, these cardiomyocytes were used to determine the rate of cardiac cell death in cells treated with Doxorubicin and BNS-22 concurrently compared to cells treated with Doxorubicin alone. Cell viability was measured by luminescence assay using the CellTiter-Glo kit. Cell viability was measured 72 hours after the administration of Vehicle (control) or BNS-22 or doxorubicin or doxorubicin and BNS-22.

Results:

Cardiomyocytes (H9C2) were grown following standard cell culture conditions. Cells which were treated with both Doxorubicin and BNS-22 together and the cells treated with only BNS-22 suffered considerably less cell loss than the cells treated with Doxorubicin alone.

Conclusions:

These preliminary results suggest that BNS-22 helps to alleviate the cardiotoxic effects of Doxorubicin. This experiment provides some evidence for the use of Topoisomerase inhibitors in the treatment of doxorubicin induced cardiotoxicity. Further cell viability assays using this drug will be performed to substantiate current findings.