Key result
Calophyllolide at 150 μg/mL improved H9c2 cell viability to 99% at 72 hours compared to 30% with doxorubicin alone, and significantly reduced doxorubicin-induced LDH and ROS activity.
Why the study?
The study aimed to examine the in vitro antioxidant potential, acute toxicity, and in vitro cardioprotective activity of Calophyllolide against Doxorubicin-mediated myocardial damage.
Does Calophyllolide prevent Doxorubicin-induced myocardial damage in H9c2 cells and rat models?
Does Calophyllolide prevent Doxorubicin-induced myocardial damage in H9c2 cells and rat models?
Absolute Event Rate: 99% vs 30%
Calophyllolide shows potential as a cardioprotective agent against doxorubicin-induced myocardial damage by reducing oxidative stress and improving cell viability in preclinical models.
Hypothesis-generating for calophyllolide in doxorubicin cardiotoxicity; leaves open clinical translation from in vitro/animal data.
This study aimed to examine in vitro antioxidant, acute toxicity studies and in vitro cardioprotective activity of Calophyllolide against Doxorubicin-mediated myocardial damage on H9c2. The anti-oxidant potential of Calophyllolide was evaluated by performing DPPH free radical scavenging assay and NO free radical scavenging assay. The Doxorubicin (DOX) induced hepatotoxicity studies were performed on female rats (130-160 g) and were administered Calophyllolide doses (5, 50, 200, 2000 mg/kg) orally. The rats were monitored for two weeks for signs of toxicity, and haematological and biochemical parameters were assessed post-experiment using respective analyzers. The results suggest that the doxorubicin-treated cells exhibited 60%, 48%, and 30% viability after 24, 48, and 72 hrs, respectively, compared to the normal group. Cells treated with DOX + Calophyllolide at 50 μg/mL showed 68%, 52%, and 60% viability after the same time points. Treatment with DOX + Calophyllolide at 100 μg/mL significantly increased cell viability to 78%, 81%, and 84%, while DOX + Calophyllolide at 150 μg/mL further improved viability to 90%, 98%, and 99%, indicating that Calophyllolide protects the heart muscle from DOX-induced cardiac toxicity. Doxorubicin administration significantly increased LDH activity (162%) compared to the control group, but Calophyllolide at 100 μg/mL and 150 μg/mL significantly reduced LDH activity to 122% and 70%, respectively, suggesting protection against DOX-induced cardiac damage. Similarly, doxorubicin significantly elevated ROS activity (160%) compared to the control group, while Calophyllolide at 100 μg/mL and 150 μg/mL reduced ROS levels to 98% and 78%, respectively, indicating protection against DOX-induced oxidative cardiac damage. This study underscores the potential of Calophyllolide as a candidate for further investigation as a cardio-protective agent.
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Namathoti et al. (2024) studied Doxorubicin-induced myocardial damage. Calophyllolide vs. Doxorubicin alone was evaluated on Cell viability at 72 hours. Calophyllolide at 150 μg/mL improved H9c2 cell viability to 99% at 72 hours compared to 30% with doxorubicin alone, and significantly reduced doxorubicin-induced LDH and ROS activity.
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