The Growth Inhibitory Effect of Resveratrol and Gallic Acid on Prostate Cancer Cell Lines Through the Alteration of Oxidative Stress Balance: The Interplay Between , and Genes

Overview

Journal Anticancer Agents Med Chem

Publisher Bentham Science Publishers

Specialties Chemistry
Oncology

Date 2024 Jul 10

PMID 38984567

Authors

Delaram Moghadam

Reza Zarei

Amirabbas Rostami

Mohammad Samare-Najaf

Rozita Ghojoghi

Amir Savardashtaki

Morteza Jafarinia

Sina Vakili

Cambyz Irajie

Affiliations

Soon will be listed here.

Abstract

Background: The association between oxidative stress and prostate cancer (PC) has been demonstrated both epidemiologically and experimentally. Balance in reactive oxygen species (ROS) levels depends on multiple factors, such as the expression of , and genes. Natural polyphenols, such as resveratrol (RSV) and gallic acid (GA), affect cellular oxidative profiles.

Objective: The present study investigated the possible effects of GA and RSV on the oxidative profiles of PC3 and DU145 cells, as well as , and gene expression to achieve an understanding of the mechanisms involved.

Methods: PC3 and DU145 cells were treated with ascending concentrations of RSV and GA for 72 h. Then cell growth and mRNA expression of , and genes were analyzed by real-time PCR. Various spectrophotometric analyses were performed to measure oxidative stress markers.

Results: RSV and GA significantly decreased the growth of PC3 and DU145 cells compared to the control group in a concentration-dependent manner. RSV and GA also decreased ROS production in PC3 cells, but in DU145 cells, only the latter polyphenol significantly decreased ROS content. In addition, RSV and GA had ameliorating effects on SOD, GR, GPX, and CAT activities and GSH levels in both cell lines. Also, RSV and GA induced HO- 1 and Nrf2 gene expression in both cell lines. BACH1 gene expression was induced by RSV only at lower concentrations, in contrast to GA in both cell lines.

Conclusion: Our data suggest that RSV and GA can prevent the growth of prostate cancer cells by disrupting oxidative stress-related pathways, such as changes in , and gene expression.

Citing Articles

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PMID: 39164783 PMC: 11334420. DOI: 10.1186/s13020-024-00982-2.

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