Baicalin Attenuates IL-17-Mediated Acetaminophen-Induced Liver Injury in a Mouse Model

• Published in: PloS one 2016-11, Vol.11 (11), p.e0166856
• Main Authors: Liao, Chia-Chih, Day, Yuan-Ji, Lee, Hung-Chen, Liou, Jiin-Tarng, Chou, An-Hsun, Liu, Fu-Chao
• Format: Article
• Language: English
• Subjects: Acetaminophen; Acetaminophen - adverse effects; Adhesive joints; Alanine; Alanine Transaminase - blood; Analgesics; Analysis; Anesthesiology; Animal tissues; Animals; Attenuation; Baicalin; Biology and Life Sciences; Chemical and Drug Induced Liver Injury - blood; Chemical and Drug Induced Liver Injury - drug therapy; Chemical and Drug Induced Liver Injury - enzymology; Chemical and Drug Induced Liver Injury - pathology; Cytokines; Disease Models, Animal; Flavonoids - pharmacology; Flavonoids - therapeutic use; Flow Cytometry; Hepatitis; Hepatology; Herbal medicine; Hospitals; House mouse; Immunohistochemistry; Inflammation; Inflammatory bowel disease; Inflammatory diseases; Injection; Injuries; Injury analysis; Interleukin 17; Interleukin 6; Interleukin-17 - metabolism; Interleukin-6 - metabolism; Kinases; Laboratory animals; Liver; Liver - drug effects; Liver - metabolism; Liver - pathology; Liver diseases; Liver Regeneration - drug effects; Lymphocytes; Male; Malondialdehyde; Malondialdehyde - metabolism; Mathematical models; Medical research; Medicine; Medicine and Health Sciences; Mice; Mice, Inbred C57BL; Neutrophils; Overdose; Parameters; Peroxidase; Peroxidase - metabolism; Receptors, Antigen, T-Cell, gamma-delta - metabolism; Recruitment; Research and Analysis Methods; Rodents; Superoxide Dismutase - metabolism; T cells; T-Lymphocytes - drug effects; T-Lymphocytes - metabolism; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-α
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0166856

IL-17 has been shown to be involved in liver inflammatory disorders in both mice and humans. Baicalin (BA), a major compound extracted from traditional herb medicine (Scutellariae radix), has potent hepatoprotective properties. Previous study showed that BA inhibits IL-17-mediated lymphocyte adhesion and downregulates joint inflammation. The aim of this study is to investigate the role of IL-17 in the hepatoprotective effects of BA in an acetaminophen (APAP)-induced liver injury mouse model. Eight weeks male C57BL/6 (B6) mice were used for this study. Mice received intraperitoneal hepatotoxic injection of APAP (300 mg/kg) and after 30 min of injection, the mice were treated with BA at a concentration of 30 mg/kg. After 16 h of treatment, mice were killed. Blood samples and liver tissues were harvested for analysis of liver injury parameters. APAP overdose significantly increased the serum alanine transferase (ALT) levels, hepatic activities of myeloperoxidase (MPO), expression of cytokines (TNF-α, IL-6, and IL-17), and malondialdehyde (MDA) activity when compared with the control animals. BA treatment after APAP administration significantly attenuated the elevation of these parameters in APAP-induced liver injury mice. Furthermore, BA treatment could also decrease hepatic IL-17-producing γδT cells recruitment, which was induced after APAP overdose. Our data suggested that baicalin treatment could effectively decrease APAP-induced liver injury in part through attenuation of hepatic IL-17 expression. These results indicate that baicalin is a potential hepatoprotective agent.