JGH open : an open access journal of gastroenterology and hepatology · 2026
Daikenchuto and Processed Ginger Alleviate Liver Ischemia-Reperfusion Injury by Enhancing Anti-Inflammatory Effects and HO-1 Production.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Saga Kenichi, Uchida Yoichiro, Kawamoto Hiroshi, Hirao Hirofumi, Umino Yosuke, Ito Masaaki, Kidoguchi Yuki, Kawasoe Junya, Tanaka Kosuke, Kadono Kentaro, Kageyama Shoichi, Taura Kojiro, Terajima Hiroaki, Watanabe Takeshi, Hatano Etsuro
Аннотация
BACKGROUND AND AIM: Daikenchuto (DKT), a Kampo medicine, is widely used in surgical practice because of its pro-motility effects on the gastrointestinal tract. Although its anti-inflammatory effects in the gastrointestinal tract have been well documented, its role in hepatic ischemia-reperfusion injury (IRI) remains unclear. This study investigated the protective effects of DKT and its individual components against hepatic IRI.
METHODS: Male C57BL/6 mice were fed a diet containing 3.6% DKT or its individual herbal components for 1 week before 60 min of partial hepatic ischemia. Liver injury was evaluated based on serum liver enzyme levels, histology, and TUNEL staining. Portal venous adrenomedullin (ADM) levels and hepatic heme oxygenase-1 (HO-1) expression were also assessed. In vitro, peritoneal macrophages were stimulated with High Mobility Group Box 1 (HMGB1) to examine the effects of DKT and 6-shogaol (6SG).
RESULTS: DKT significantly reduced serum alanine aminotransferase levels, necrotic area, and hepatocyte apoptosis compared to the control. Although single-herb doses equivalent to those in the DKT formula did not confer protection, a threefold dose of processed ginger reproduced the hepatoprotective effects of DKT. DKT did not increase portal ADM levels. In contrast, both DKT and 6SG significantly upregulated HO-1 expression in vivo and suppressed the production of inflammatory cytokines in HMGB1-stimulated macrophages in vitro.
CONCLUSION: DKT attenuates liver IRI via HO-1 induction and suppression of macrophage-mediated inflammation, rather than via ADM elevation. These protective effects may be mediated, at least in part, by processed ginger.
METHODS: Male C57BL/6 mice were fed a diet containing 3.6% DKT or its individual herbal components for 1 week before 60 min of partial hepatic ischemia. Liver injury was evaluated based on serum liver enzyme levels, histology, and TUNEL staining. Portal venous adrenomedullin (ADM) levels and hepatic heme oxygenase-1 (HO-1) expression were also assessed. In vitro, peritoneal macrophages were stimulated with High Mobility Group Box 1 (HMGB1) to examine the effects of DKT and 6-shogaol (6SG).
RESULTS: DKT significantly reduced serum alanine aminotransferase levels, necrotic area, and hepatocyte apoptosis compared to the control. Although single-herb doses equivalent to those in the DKT formula did not confer protection, a threefold dose of processed ginger reproduced the hepatoprotective effects of DKT. DKT did not increase portal ADM levels. In contrast, both DKT and 6SG significantly upregulated HO-1 expression in vivo and suppressed the production of inflammatory cytokines in HMGB1-stimulated macrophages in vitro.
CONCLUSION: DKT attenuates liver IRI via HO-1 induction and suppression of macrophage-mediated inflammation, rather than via ADM elevation. These protective effects may be mediated, at least in part, by processed ginger.