Fundamental Toxicological Sciences

Paper Details

Fundamental Toxicological Sciences
Vol. 6 No. 1 February 06, 2019 p.25-29
Letter
Protective effect of the Kampo formula “Juzen-taiho-to” on isoniazid- and rifampicin-induced hepatotoxicity in mice
  • Hiroki Yoshioka (Department of Pharmacy, College of Pharmacy, Kinjo Gakuin University / h-yoshioka@kinjo-u.ac.jp)
  • Tohru Maeda (Department of Pharmacy, College of Pharmacy, Kinjo Gakuin University / phmaeda@kinjo-u.ac.jp)
Hiroki Yoshioka 1) , Shiori Fukaya 1) , Sarah Tominaga 1) , Akito Nagatsu 1) , Nobuhiko Miura 2) , Tohru Maeda 1)
1) Department of Pharmacy, College of Pharmacy, Kinjo Gakuin University , 2) Division of Health Effects Research, Japan National Institute of Occupational Safety and Health
Keywords: Isoniazid, Rifampicin, Hepatic injury, Anti tubercular drug
Abstracts

The aim of this study was to investigate whether the Japanese herbal medicine Juzentaiho-to (JTX) showed attenuating effects on isoniazid- and rifampicin-induced liver injury. Seven-weekold male Institute of Cancer Research mice were orally administered JTX or saline once a day at 9:00 for 3 days. Additionally, the mice received a mixture of 80 mg/kg isoniazid and 160 mg/kg rifampicin (10 mL/kg) via intraperitoneal injection three times (at 19:30) per 24 hr period. Twenty-four hours after the last administration of isoniazid/rifampicin, the mice in each group were sacrificed and blood was removed to obtain the plasma and livers. Mice that had received isoniazid/rifampicin showed high plasma levels of alanine aminotransferase, aspartate aminotransferase, and interleukin-6. In addition, the mice injected with isoniazid/rifampicin displayed increased hepatic lipid peroxidation and receptor-interacting protein-1 and -3 levels. Treatment with JTX prevented an isoniazid/rifampicin-induced increase in levels of alanine aminotransferase and aspartate aminotransferase, lipid peroxidation, and receptor-interacting protein changes. Our results suggest that JTX protects against isoniazid/rifampicin-induced hepatic injury by modulating oxidative stress and inflammatory responses.