Evaluation of Cytotoxic Activity of Betanin Against U87MG Human Glioma Cells and Normal Human Lymphocytes and Its Anticancer Potential Through Mitochondrial Pathway

Abstract

Recent studies revealed an antioxidant activity and anticancer efficiency of betanin. In this study, we investigated the cytotoxic effects and the possible mechanisms of betanin-induced apoptosis against U87MG human glioma cells and compared the results to those of human normal lymphocytes. MTT assay, caspase-3 activation assays in cells and succinate dehydrogenases (SDH), mitochondrial swelling, reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and cytochrome C release assays in isolated mitochondria were obtained from U87MG human glioma cells and noncancerous human lymphocytes The results illustrated the significant cytotoxic effect of betanin on U87MG human glioma cells, with a concentration value that inhibits 50% of the cell growth of 7 µg/ml after 12 h of treatment. MTT assay demonstrated that the betanin is selectively toxic to U87MG human glioma cells, and betanin induced cell apoptosis via activation of caspase-3 along with modulation of apoptosis-related mitochondria. Meanwhile, betanin selectively increased ROS formation, mitochondria swelling, MMP decrease, and cytochrome c release in cancerous mitochondria but in normal mitochondria. Based on the evidence obtained from this study, it is concluded that the betanin is a promising natural compound to fight U87MG human glioma cells via induction of apoptosis through activation of intrinsic pathways.

Acknowledgments

The data provided in this article was extracted from the Pharm D. thesis of Dr. Tannaz Bahiraei. The thesis was conducted under supervision of Prof. Jalal Pourahmad at Department of Toxicology and Pharmacology, Faculty of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran.

Disclosure statement

The authors declare that they have no conflict of interest.

Authors’ Contributions

A. Salimi contributed to interpretation, drafted manuscript, and critically revised manuscript; T. Bahiraei contributed to acquisition of data; Sana Ahdeno and Saba Vatanpour contributed to analysis of data; J. Pourahmad contributed to conception and design and critically revised manuscript. All authors gave final approval and agreed to be accountable for all aspects of work ensuring integrity and accuracy.

Additional information

Funding

This work was supported by Shahid Beheshti University of Medical Sciences, Deputy of Research.