Emodin, an anthraquinone derivative, protects against gamma radiation-induced toxicity by inhibiting DNA damage and oxidative stress

Abstract

Purpose: In the present study, we explored the modulatory effect of emodin (1,3,8-trihydroxy-6-methylanthraquinone, C₁₅H₁₀O₅) against gamma radiation-induced DNA damage and oxidative stress in acellular and cellular systems, respectively.

Materials and methods: For cellular systems, concanavalin A (ConA)-stimulated murine splenocytes were used. Cytotoxic effect of emodin (0–400 μM), radiation (3–12 Gy) and emodin + radiation was measured by MTT [3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay. Gamma radiation (3–12 Gy)-induced production of reactive oxygen species (ROS), an increase in nitric oxide (NO) level and its inhibition by emodin were estimated by DCFDA (2ʹ,7ʹ-dichlorofluorescein diacetate) and Griess regent, respectively. Analysis of radiation-induced apoptosis was performed using flow cytometery and acridine orange/ethidium bromide staining. DNA damage was evaluated in acellular system using pBR322 plasmid relaxation assay.

Results: Emodin was able to effectively scavenge radiation- induced free radicals (ROS and NO) in murine splenocytes. Radiation-induced apoptosis and cell death was also inhibited by emodin pre-treatment. It could significantly prevent radiation-induced DNA damage.

Conclusions: Protection against gamma radiation-induced cell death and DNA damage by emodin could be attributed to its free radical scavenging activity. The present study is the first report of the radioprotective role of emodin in mammalian cells.

Keywords::

• Gamma-radiation
• emodin
• ROS
• apoptosis
• DNA damage

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

ABT is grateful to University Grants Commission (UGC), India for funding this project (UGC-02100113-501). Grant received from Jawaharlal Nehru University, India, in the form of UGC-Networking and Department of Science and Technology-Purse (DST-08090712-462) is also gratefully acknowledged. RS is thankful to UGC for providing financial support in the form of project fellowship.