Selenium Donor Inhibited Hepatitis B Virus Associated Hepatotoxicity via the Apoptosis and Ferroptosis Pathways
Jingdong Shi, Zhen Liu, Weina Li, Di Wang- Cancer Research
- Cell Biology
- Molecular Medicine
- General Medicine
- Pathology and Forensic Medicine
Background and Aim. Selenium possesses anticancer and antiviral properties, but its mechanism of action remains unclear. Especially, the impact of selenium on hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) remains unknown. This study aimed to investigate the inhibitory properties of selenium on HBV replication and its related hepatotoxicity via the apoptosis and ferroptosis pathways. Methods. The serum selenium level was determined in 45 patients with HBV-positive HCC (HBV+-HCC group), 45 patients with chronic hepatitis B virus infection (CHB group), and 45 healthy cases (HC group). The sodium selenite (Na2SeO3)-treated HepG2.2.15 cells were used to observe the regulatory role of selenium on HBV replication. D-GalN/erastin-added HL7702 was used to determine the regulatory roles of Na2SeO3 on hepatotoxicity or hepatocyte ferroptosis. The wild-type (WT) C57BL/6 mice and HBx-Tg mice were received lipopolysaccharide (LPS)/D-GalN, together with or without Na2SeO3 administration for indicated period. Following euthanasia, the blood and liver tissue samples were collected, and specific markers were evaluated subsequently. Results. The serum selenium level was downregulated in patients with HBV-positive HCC (HBV+-HCC group) (57.2 ± 22.5 μg/L vs. 91.8 ± 43.9 μg/L,