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Original Articles

Hesperidin Induces ROS-Mediated Apoptosis along with Cell Cycle Arrest at G2/M Phase in Human Gall Bladder Carcinoma

, , , ORCID Icon, &
Pages 676-687 | Received 16 Feb 2018, Accepted 18 Jul 2018, Published online: 28 Sep 2018
 

Abstract

A natural predominant flavonoid hesperidin rich in citrus fruits exhibits multifunctional medicinal properties. The anticancerous potential of hesperidin has been widely explored; however, the gall bladder carcinoma (GBC) still remains untouched due to the unavailability of efficient experimental model. The aim of our study was to identify the apoptotic and antiproliferative potential of hesperidin in GBC. The promising efficacy of hesperidin was assessed through the generation of reactive oxygen species (ROS), cellular apoptosis, and loss of mitochondrial membrane potential (MMP) in the primary cells generated from surgically removed cancerous gall bladder tissues. Moreover, cell cycle analysis and caspases-3 activity were performed to confirm the apoptosis inducing potential of hesperidin. Results revealed that hesperidin exposure for 24 h at a dose of 200 µM reduced the cell proliferation of GBC cells significantly. In addition, hesperidin treatment further resulted in an increased ROS generation and nuclear condensation at the same dose. Caspase-3 activation and cell cycle arrest at G2/M phase were also accelerated in a dose-dependent manner. Together, these results suggest that hesperidin can be considered as a potential anticancerous compound for the treatment of GBC. Furthermore, evaluation of the pharmacological aspects of hesperidin is desirable for drug development.

Acknowledgments

We thank Integral University communication cell, Lucknow, UP, India, for quick and crisp review of the manuscript (IU/R&D/2017-MCN 000220) and providing insightful comments.

Disclosure Statement

I confirm that this research article authored by me/us is an original and genuine research work. It has neither been submitted for publication nor published elsewhere in any print/electronic form.

Additional information

Funding

Support in the form of grant from the Department of Science and Technology, WOS-A, is highly acknowledged.

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