Shigyakusan extract attenuates enhanced hepatic neutrophil infiltration and oxidative stress with progression of α-naphthylisothiocyanate-induced liver injury in rats

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  • OHTA Yoshiji
    Departments of Chemistry, School of Medicine, Fujita Health University
  • KONGO-NISHIMURA Mutsumi
    Department of Pediatric Surgery, School of Medicine, Fujita Health University
  • HAYASHI Takahiro
    Department of Pharmacy, Fujita Health University Hospital
  • KITAGAWA Akira
    Department of Nutrition, Faculty of Wellness, Chukyo Women's University
  • MATSURA Tatsuya
    Division of Medical Biochemistry, Department of Pathophysiology and Therapeutic Science, Faculty of Medicine, Tottori University
  • HASHIMOTO Takashi
    Department of Pediatric Surgery, School of Medicine, Fujita Health University
  • YAMADA Kazuo
    Division of Medical Biochemistry, Department of Pathophysiology and Therapeutic Science, Faculty of Medicine, Tottori University

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  • Shigyakusan extract attenuates enhanced hepatic neutrophil infiltration and oxidative stress with progression of a naphthylisothiocyanate induced liver injury in rats

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In the present study, we examined whether shigyakusan extract, a traditional Kampo medicine, attenuates enhanced hepatic neutrophil infiltration and oxidative stress with the progression of α-naphthylisothiocyanate (ANIT)-induced liver injury in rats. Rats were treated once with ANIT (75 mg/kg body weight, i.p.). Liver injury with cholestasis occurred 24 h after ANIT treatment and progressed at 48 h. A spray-dried material of shigyakusan extract (SGS) (0.15, 0.75 or 1.5 g/kg body weight, p.o.) administered at 24 h after ANIT treatment prevented the progression of ANIT-induced liver injury dose-dependently. At 24 h after ANIT treatment, the treated rats showed increases in hepatic lipid peroxide (LPO) and reduced glutathione (GSH) contents and myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, and decreases in hepatic superoxide dismutase (SOD) and glutathione reductase (GSSG-R) activities. At 48 h after ANIT treatment, the treated rats showed enhanced changes in hepatic LPO content and MPO, SOD, and GSSG-R activities except GSH content and decreases in hepatic catalase, Se-glutathione peroxidase, and glucose-6-phosphate dehydrogenase activities. SGS administered at 24 h after ANIT treatment attenuated the ANIT-induced changes in hepatic LPO and GSH content and MPO, catalase, and Se-glutathione peroxidase activities except SOD, GSSG-R, and glucose-6-phosphate dehydrogenase activities at 48 h dose-dependently. These results indicate that orally administered SGS attenuates enhanced hepatic neutrophil infiltration and oxidative stress with liver injury progression and increased hepatic GSH content at the progressed stage of liver injury in rats treated with ANIT, which could contributes to its therapeutic effect on this liver injury.

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