Cytoprotective Effect of Gallic Acid against Injuries Promoted by Therapeutic Ionizing Radiation in Preosteoblast Cells

• Published in: International journal of molecular and cellular medicine Vol. 13; no. 1; pp. 19 - 28
• Main Authors: Leite, Renata Sousa, da Rocha, Rogério Gonçalves, Lima Tabosa, Angeliny Tamiarana, Batista Gomes, Emisael Stênio, Santiago, Laís, Rodrigues, Danillo Costa, Sousa Santos, Sérgio Henrique, Sena Guimarães, André Luiz, Farias, Lucyana Conceição
• Format: Journal Article
• Language: English
• Published: Iran Babol University of Medical Sciences 2024
• Subjects: Original; radiotherapy; osteoradion-ecrosis; osteonecrosis; Gallic acid; Antioxidant; ionizing radiation
• ISSN: 2251-9637; 2251-9645
• DOI: 10.22088/IJMCM.BUMS.13.1.19

Gallic acid (GA) is a powerful antioxidant extracted from plants of the Brazilian Cerrado. Oxidative stress plays an important role in the occurrence of radiation-induced osteonecrosis in patients treated for head and neck cancer. There is a need to develop research aimed at developing complementary therapies to prevent or reverse bone damage. The aim of the present study was to investigate the effect of GA in preosteoblasts exposed to therapeutic ionizing radiation. MC3T3-E1 preosteoblast cells were treated with 10 µM GA and exposed to 6 Gy ionizing radiation. We performed
assays of cell proliferation, oxidative stress analysis by detection of reactive oxygen species, and alkaline phosphatase assay. GA at lower concentrations was able to significantly increase proliferation and inhibit radiation-induced generation of reactive oxygen species in osteoblast precursor cells, despite ionizing radiation-induced injury. Furthermore, GA significantly increased alkaline phosphatase at a dose of 6 Gy. The findings suggested that GA could attenuate ionizing radiation-induced injuries in osteoblast precursor cells. Moreover,
studies are needed to better investigate the role of GA in osteonecrosis, especially in cancer patients undergoing radiotherapy or taking antiresorptive drugs.