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Morphine Attenuated the Cytotoxicity Induced by Arsenic Trioxide in H9c2 Cardiomyocytes
Hossein Amini-Khoei1,2, Mir-Jamal Hosseini3, Majid Momeny4
1Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Abstract:
Arsenic trioxide (ATO) is an efficient drug for the treatment of the patients with acute promyelocytic leukemia (APL). Inhibition of proliferation as well as apoptosis, attenuation of migration, and induction of differentiation in tumor cells are the main mechanisms through which ATO acts against APL. Despite advantages of ATO in treatment of some malignancies, certain harmful side effects, such as cardiotoxicity, have been reported. It has been well documented that morphine has antioxidant, anti-apoptotic, and cytoprotective properties and is able to attenuate cytotoxicity. Therefore, in this study, we aimed to investigate the protective effects of morphine against ATO toxicity in H9c2 myocytes using multi-parametric assay including thiazolyl blue tetrazolium bromide (MTT) assay, reactive oxygen species (ROS) generation, caspase 3 activity, nuclear factor kappa B (NF-κB) phosphorylation assay, and expression of apoptotic markers. Our results showed that morphine (1 μM) attenuated cytotoxicity induced by ATO in H9c2 cells. Results of this study suggest that morphine may have protective properties in management of cardiac toxicity in patients who receive ATO as an anti-cancer treatment.
Insights
Morphine demonstrated protective effects against arsenic trioxide (ATO) toxicity in heart cells. This suggests morphine may help manage cardiac side effects in patients undergoing ATO cancer treatment.
Area of Science:
- Pharmacology
- Cardiology
- Oncology
Background:
- Arsenic trioxide (ATO) is a key drug for acute promyelocytic leukemia (APL), working by inhibiting proliferation and inducing apoptosis.
- ATO treatment can cause cardiotoxicity, a significant harmful side effect.
- Morphine possesses known antioxidant, anti-apoptotic, and cytoprotective properties.
Purpose of the Study:
- To investigate the potential cardioprotective effects of morphine against ATO-induced toxicity.
- To evaluate morphine's impact on cellular damage markers in cardiac myocytes exposed to ATO.
Main Methods:
- H9c2 myocytes were treated with ATO and varying concentrations of morphine.
- Multi-parametric assays were employed, including MTT assay, reactive oxygen species (ROS) generation, caspase-3 activity, NF-κB phosphorylation, and apoptotic marker expression.
Main Results:
- Morphine (1 μM) significantly attenuated the cytotoxicity induced by ATO in H9c2 cells.
- Morphine reduced ATO-induced ROS generation and caspase-3 activity.
- Morphine modulated the expression of apoptotic markers, indicating a protective mechanism.
Conclusions:
- Morphine exhibits protective effects against arsenic trioxide-induced cardiotoxicity in vitro.
- These findings suggest a potential therapeutic role for morphine in mitigating cardiac adverse events associated with ATO cancer therapy.
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