Protective effect of the Kampo formula “Juzen-taiho-to” on isoniazid- and rifampicin-induced hepatotoxicity in mice

Abstract

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.

Intron retention as a new pre-symptomatic marker of aging and its recovery to the normal state by a traditional Japanese multi-herbal medicine

“…Among the 11 IR-recovered loci that overlapped between liver and blood (Figure 6D), Faah is connected with macrophage function through lipid metabolism (Yoshioka et al, 2019), and Gdi1 is connected with interferon-γ activity through innate immunity (Fukaya et al, 2018). Among 12 IR-recovered loci that overlapped between liver and bone (Figure 6D), Sirt1 is positively involved in macrophage self-renewal activity, during which it functions to increase their proliferative capacity during bone marrow-derived macrophage differentiation (Imperatore et al, 2017).…”