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Sesamol prevents doxorubicin-induced oxidative damage and toxicity on H9c2 cardiomyoblasts
Pawan G Nayak1, Piya Paul, Punit Bansal
1Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal University, Manipal, Karnataka, India.
Objectives:
Exposure to toxicants like doxorubicin (Dox) damages cellular components by generating reactive oxygen species (ROS). This can be attenuated using free radical scavengers and/or antioxidants.
Methods:
Dox-exposed cardiac myoblasts (H9c2 cells) were treated with sesamol (12.5, 25 and 50 μm), a natural phenolic compound. Intracellular ROS inhibition, cell viability and analysis of antioxidant and biochemical markers such as superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase, reduced/oxidized glutathione, lipid peroxidation and protein carbonyl content were performed. The effect of sesamol treatment on the cytotoxic and genotoxic parameters was studied by monitoring the signalling proteins involved in the apoptotic pathway.
Key Findings:
Dox triggered cellular and genetic damage by increasing levels of intracellular ROS, thereby decreasing cell viability and increasing apoptosis. Sesamol reversed the cytotoxic and genotoxic effects of Dox. In addition, sesamol attenuated the pro-apoptotic proteins and improved the anti-apoptotic status. Sesamol pre-treatment also alleviated the disturbed antioxidant milieu by preventing ROS production and improving endogenous enzyme levels.
Conclusions:
Among the different doses tested, 50 μm of sesamol showed maximum protection against Dox-induced oxidative damage. This reflects the significance of sesamol in ameliorating the deleterious effects associated with cancer chemotherapy.
Insights
Sesamol, a natural antioxidant, protects against doxorubicin-induced oxidative damage in cardiac cells. It reverses cytotoxic and genotoxic effects by reducing reactive oxygen species (ROS) and improving antioxidant enzyme levels.
Area of Science:
- Cardiovascular Toxicology
- Oxidative Stress Research
- Pharmacology
Background:
- Doxorubicin (Dox) chemotherapy induces cellular damage via reactive oxygen species (ROS).
- Antioxidants and free radical scavengers can mitigate this Dox-induced toxicity.
Purpose of the Study:
- To investigate the protective effects of sesamol, a natural phenolic compound, against doxorubicin-induced oxidative damage in cardiac myoblasts (H9c2 cells).
Main Methods:
- H9c2 cells were exposed to doxorubicin and treated with varying concentrations of sesamol.
- Assessed intracellular ROS, cell viability, antioxidant enzyme activity (superoxide dismutase, catalase, glutathione-S-transferase, glutathione peroxidase), lipid peroxidation, and protein carbonyl content.
- Monitored apoptotic pathway signaling proteins to evaluate cytotoxic and genotoxic effects.
Main Results:
- Doxorubicin increased intracellular ROS, reduced cell viability, and elevated apoptosis.
- Sesamol treatment reversed doxorubicin's cytotoxic and genotoxic effects.
- Sesamol attenuated pro-apoptotic proteins, enhanced anti-apoptotic status, and improved the antioxidant defense system by preventing ROS production.
Conclusions:
- Sesamol effectively ameliorates doxorubicin-induced oxidative damage in cardiac cells.
- A concentration of 50 μm sesamol demonstrated maximal protective effects against Dox-induced toxicity.
- Sesamol holds significance in mitigating chemotherapy-related adverse effects.
