Detailed Abstract
[Liver Poster Presentation 4]
[LV PP 4-4] Crepidiastrum denticulatum extract ameliorates hepatic ischemia-reperfusion injury in mice via an autophagy mechanism
Hyuk Jai JANG*1, Gyhye YOO2, Chu Won NHO2
1Surgery, Ulsan University, Gangneung Asan Hospital, Korea
2Natural Product Informatics Research Center,, Korea Institute of Science and Technology (KIST), Gangneung, Korea
Introduction : Crepidiastrum denticulatum (CD), which is a traditionally consumed plant in Korea, is already identified as an effective agent for liver protection owing to its antioxidant and anti-inflammatory effects. Hepatic ischemia/reperfusion injury (hepatic IRI) is a pathological problem in surgical procedures, including hepatic resection and transplantation. Several factors involved in the mechanism underlying hepatic IRI have been investigated. However, preventive and/or therapeutic methods for hepatic IRI are yet to be developed. In this study, we investigated the protective effect of CD against hepatic IRI.
Methods : Partial (70%) hepatic IRI was induced in male C57BL/6 mice by portal triad pedicle occlusion for 45 min followed by reperfusion for 6 h. CD (75 mg/kg BW, oral) was administered 5 days before the IRI.
Results : The results showed that hepatic IRI increased the blood levels of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase, which are reasonably sensitive liver damage indicators. These markers were reduced by CD treatment. Histological examination of H&E-stained liver tissues showed uniformly distributed IRI-affected nuclei, and the CD-treated group showed decreased histopathological scores compared to the IRI group. Western blotting of liver showed that hepatic IRI decreased autophagy and antioxidant markers, while CD treatment increased these markers. Additionally, IRI increased the levels of inflammatory molecules, including NFκB and nitric oxide synthase, but CD administration suppressed these levels thereby inhibiting nitric oxide (NO) production.
Conclusions : : These data suggest that CD extract has protective effects against hepatic IRI via autophagy-dependent cell survival mechanism, resulting from antioxidant effects, including NO suppression.
Methods : Partial (70%) hepatic IRI was induced in male C57BL/6 mice by portal triad pedicle occlusion for 45 min followed by reperfusion for 6 h. CD (75 mg/kg BW, oral) was administered 5 days before the IRI.
Results : The results showed that hepatic IRI increased the blood levels of aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase, which are reasonably sensitive liver damage indicators. These markers were reduced by CD treatment. Histological examination of H&E-stained liver tissues showed uniformly distributed IRI-affected nuclei, and the CD-treated group showed decreased histopathological scores compared to the IRI group. Western blotting of liver showed that hepatic IRI decreased autophagy and antioxidant markers, while CD treatment increased these markers. Additionally, IRI increased the levels of inflammatory molecules, including NFκB and nitric oxide synthase, but CD administration suppressed these levels thereby inhibiting nitric oxide (NO) production.
Conclusions : : These data suggest that CD extract has protective effects against hepatic IRI via autophagy-dependent cell survival mechanism, resulting from antioxidant effects, including NO suppression.
SESSION
Liver Poster Presentation 4
E-Session 7/27 ~ 7/29 ALL DAY