Development of Basic Technologies for the Domestic Cultivation of Herbal Medicine Resources at KIOM (Korea Institute of Oriental Medicine)

Abstract

Purpose: To investigate the hepatoprotective effects of Panax ginseng C.A Meyer extract (PGE) and its corresponding mechanisms using radiation-induced liver disease. Methods: C57/BL6 mice were orally administered with PG (0, 25, 50 or 100mg/kg) or intraperitonealy injected melatonin (20mg/ kg) for 4 consecutive days before 15Gy X-ray radiation exposure 1 hr after the last administration of PGE. Hepatic triglyceride (TG), histopathology, oxidative stress parameters, antioxidant components, inflammatory cytokines, and apoptosis signals were examined at 10 days after radiation. Results: The irradiation markedly altered the steatotic alteration by histological examination andmeasuring hepatic TG in the tissue. Those alterations, however, were significantly attenuated by PGE. Immunohistochemistry examination showed the 4-hydroxynonenal signals were enhanced by radiation, while pre-treatment with PGE remarkably reduced them. Pretreatment with PGE not only markedly exerted to reduce both total reactive oxygen species and lipid peroxidation in hepatic tissue level. Radiation cased remarked depletion of total glutathione (GSH) contents and decreases of antioxidant enzyme activities including superoxide distumates, catalase, and GSH-reducatse in hepatic protein levels, whereas pre-treatment with PGE significantly exerted to normalize them. Inflammatory cytokines including TNF, IL-1 and IL-6 were notably increased in hepatic tissues due to radiation, and then these were efficiently attenuated by pre-treatment with PGE. Moreover, pre-treatment with PGE significantly blocked the apoptotic signals by measuring TUNEL assay, western blot, and gene expression levels in hepatic tissue. Conclusion:Collectively, above findings evidenced that PGE beneficially prevent from RILI, and its corresponding mechanisms involved the inhibition of fat accumulation, oxidative stress, inflammatory cytokines, and apoptosis signals. Contact: Hyeong-Geug Kim, winakim@dju.kr