Evaluation of Chelidonium Majus L. Alkaloid Effect on VEGF Gene Expression and Cell Apoptosis in the Burkitt Lymphoma Cell Line

Mitra Sadeghpour  Natanzi; Masoud  Parsania; Fatemeh  Ashrafi; Mohammad Hassan  Pouriayevali

doi:10.18502/ijpho.v15i1.17280

Mitra Sadeghpour Natanzi Department of Microbiology Faculty of Biological Sciences, Islamic Azad University, North Tehran branch, Tehran, Iran.
Masoud Parsania Associate professor, Department of Microbiology, Faculty of Medicine, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Fatemeh Ashrafi Assistant professor, Department of Microbiology, Faculty of Biological Sciences, Islamic Azad University, North Tehran branch, Tehran, Iran.
Mohammad Hassan Pouriayevali Assistant professor, Department of Arboviruses and Viral Hemorrhagic Fevers (National Ref Lab), Pasteur Institute of Iran, Tehran, Iran.

DOI: https://doi.org/10.18502/ijpho.v15i1.17280

Keywords: Burkitt lymphoma, Chelidonium majus, Vascular endothelial growth factor

Abstract

Background: Burkitt lymphoma (BL) is a type of mature B-cell non-Hodgkin’s lymphoma that commonly develops in children and young adults. Vascular endothelial growth factor (VEGF) is acknowledged as a vital regulator of angiogenesis in both normal and disease states. In light of the adverse effects linked to chemical treatments, this study aimed to explore the anticancer effects of Chelidonium majus L. alkaloid on the Daudi BL cell line and to evaluate the expression of the VEGF gene.

Materials and Methods: This project was an experimental study. The cytotoxic effects of the alkaloid derived from Chelidonium majus L. on the Daudi and normal cells were evaluated using MTT assays (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide). The induction of apoptosis in cells was measured utilizing Annexin V/propidium iodide (PI) flow cytometry. Additionally, the expression levels of the VEGF gene were determined via a Real-time PCR assay. Data were entered into SPSS, version 21. Student’s t-test and ANOVA test were used for comparisons of groups.

Results: The 50% cytotoxic concentration (CC₅₀) of the alkaloid from Chelidonium majus L. was found to be 56.35µg/mL in the Daudi cell. Findings from flow cytometry aligned with those from MTT assays. Real-time PCR assay results showed a significant decrease in the VEGF gene expression (P<0.009). Effects observed after 48 hours of treatment across various concentrations of Chelidonium majus L. alkaloid demonstrated dose-dependency. However, in peripheral blood mononuclear cells (PBMCs) as a control, the alkaloid did not significantly affect the expression of the VEGF gene (P>0.05).

Conclusion: The alkaloid is derived from Chelidonium majusL. Appears to influence angiogenesis by down-regulating the VEGF gene expression, suggesting its potential as a complementary agent in chemotherapy for Burkitt lymphoma. However; further research is required to evaluate the effectiveness of the Chelidonium majusL. Extract as a definitive treatment for Burkitt lymphoma.