Role of Cyanidin 3-glucoside Extract in the Induction of Cytotoxicity and Apoptosis in a Rat Bladder Cancer Cell Line

Alubaidy, Haider Ammar; Al-Bdeery, Ali Hamid; Abdul-Adel, Esraa; Juda, Sarab A.; Abd_alameer, Taghreed Hamed; Jabir, Majid Sakhi

doi:10.31557/APJCP.2026.27.5.1795

Role of Cyanidin 3-glucoside Extract in the Induction of Cytotoxicity and Apoptosis in a Rat Bladder Cancer Cell Line

Document Type : Research Articles

Authors

¹ College of Science, Al Qadisiyah University, Iraq.

² College of Environmental Sciences, Al-Qasim Green University, Iraq.

³ College of Science, University of Babylon, Iraq.

⁴ Al-Qadisiyah Education Directorate, Ministry of Education, Iraq.

⁵ College of Applied Sciences, University of Technology, Iraq.

10.31557/APJCP.2026.27.5.1795

Abstract

Objective: This study focused on organisms that produce natural bioactive compounds that are environmentally friendly alternatives to chemical treatments. These compounds include flavonoids derived from marine algae, including anthocyanins. Cyanidin-3-glucoside (C3G) is a natural pigment-protein complex capable of inhibiting or eradicating the proliferation of malignant cells, both in vivo and in vitro. Methods: This includes the AY-27 rat (BC) bladder cancer cell line. Its potential effects on inhibiting the production of isolated rat bladder tumor cells and activating cellular pathways were studied, including cytotoxicity, apoptosis, the p53 pathway, mitochondrial wall loss pathway, and partial fusion. Result: The present study documented a peak mortality rate of 84.43% in the toxicity pathway on the maximum dose of 100 µg/ml of C3G. The minimum mortality rate of 9.45% was recorded at the maximum C3G concentration of 6.25 µg/ml. In the apoptotic process, dead cells were evaluated for DNA damage. C3G promotes mitochondrial failure in AY-27 cells via the mitochondrial pathway, leading to a reduction in mitochondrial membrane potential compared to untreated AY-27 cells. Conclusion: The study’s findings showed that C3G increased p53 gene expression in AY-27 cells during the p53 pathway. The data in the tables and figures reveal that increasing the dose or concentration of C3G over time has a lethal effect on bladder cancer cells. The results indicate that C3G promotes localized apoptosis, thereby inhibiting and slowing down the progression of bladder cancer. These findings suggest that C3G could be an active natural treatment for BC in rats, with potential for further development by international pharmaceutical companies.

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