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2000
Volume 25, Issue 4
  • ISSN: 1871-529X
  • E-ISSN: 2212-4063

Abstract

Introduction

Oroxylin A is primarily sourced from the roots of a medicinal plant commonly used in traditional Chinese medicine. It can also be found in other species. The plant's rich bioactive profile makes it a significant source of various flavonoids, including Oroxylin A.

Aims

The proposed aim of this study is to investigate anti-oxidant activity, toxicity studies and cardioprotective activity of Oroxylin-A against Doxorubicin mediated myocardial damage on H9c2.

Methods

The total phenolic content was estimated using Folin-Ciocalteu test and activity was performed using DPPH assay. Acute toxicity studies were performed according to OECD 423 guidelines. cardioprotective activity was performed on H9c2 cells and was estimated for the biomarkers.

Results

Oroxylin-A showed good antioxidant activity. No abnormalities were found in animals upon its usage, indicating that Oroxylin-A was safe at 2000 mg/kg. 150ug/ml of Oroxylin-A significantly increased the cell viability up to 99% and also decreased the LDH and ROS generation indicating that Oroxylin-A showed significant cardioprotective activity on H9c2 cells.

Discussion

Oroxylin-A demonstrated potent antioxidant and cardioprotective effects by reducing ROS generation and LDH release while enhancing H9c2 cell viability against doxorubicin-induced toxicity. Its safety at higher doses further supports its therapeutic potential. These findings highlight Oroxylin-A as a promising natural cardioprotective agent, warranting further and mechanistic studies to validate its clinical applicability.

Conclusion

This research underscores the potential of Oroxylin A as a candidate for further investigation as a cardioprotective agent. Also, the present study contributes to the growing body of knowledge aimed at identifying natural compounds that may offer protective effects against myocardial damage, providing hope for future therapeutic interventions in the field of cardiovascular medicine.

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2025-06-19
2025-12-10
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