Honokiol ameliorates radiation-induced brain injury via the activation of SIRT3

• Published in: Journal of international medical research Vol. 48; no. 10; p. 300060520963993
• Main Authors: Liao, Guixiang, Zhao, Zhihong, Yang, Hongli, Li, Xiaming
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.10.2020; Sage Publications Ltd; SAGE Publishing
• Subjects: Animals; Biphenyl Compounds; Brain - metabolism; Brain Injuries; Lignans; Oxidative Stress; Pre-Clinical Research Report; Reactive Oxygen Species; Sirtuin 3 - genetics; Sirtuin 3 - metabolism; Traumatic brain injury; Tumor necrosis factor-TNF; Zebrafish - metabolism; radiation-induced brain injury; Honokiol; sirtuin 3; reactive oxygen species; cyclooxygenase-2; ionizing irradiation
• ISSN: 0300-0605; 1473-2300
• DOI: 10.1177/0300060520963993

Objective Sirtuin 3 (SIRT3) plays a vital role in regulating oxidative stress in tissue injury. The aim of this study was to evaluate the radioprotective effects of honokiol (HKL) in a zebrafish model of radiation-induced brain injury and in HT22 cells. Methods The levels of reactive oxygen species (ROS), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1β) were evaluated in the zebrafish brain and HT22 cells. The expression levels of SIRT3 and cyclooxygenase-2 (COX-2) were measured using western blot assays and real-time polymerase chain reaction (RT-PCR). Results HKL treatment attenuated the levels of ROS, TNF-α, and IL-1β in both the in vivo and in vitro models of irradiation injury. Furthermore, HKL treatment increased the expression of SIRT3 and decreased the expression of COX-2. The radioprotective effects of HKL were achieved via SIRT3 activation. Conclusions HKL attenuated oxidative stress and pro-inflammatory responses in a SIRT3-dependent manner in radiation-induced brain injury.