Micro-MRI-based Detection of Tissue Damage in the Liver, Pancreas, and Kidney during the Early Phases of an LPS and D-Galactosamine-Induced Hepatic Injury Model in Mice*Corresponding Author: Nodoka Nago, M.D., Ph.D, Department of Molecular and Pathobiology and Cell Adhesion Biology, Graduate School of Medicine, Mie University, 2-174 Edobashi, Tsu-city, Mie 514-8507, Japan, Tel: +81-59-232-5036, Fax: +81-59-231-5209, Email: [email protected]
Received Date: Jan 21, 2020 / Accepted Date: Feb 05, 2020 / Published Date: Feb 12, 2020
Citation: Nago N, Yoneda M, Darkwah S, Kawamoto E, Park EJ, et al. (2020) Micro-MRI-based Detection of Tissue Damage in the Liver, Pancreas, and Kidney during the Early Phases of an LPS and D-Galactosamine-Induced Hepatic Injury Model in Mice. Diagn Pathol Open 5: 161.
Copyright: © 2020 Nago N, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
How tissue injuries progress among organs during LPS-induced fulminant hepatic failure remains to be elucidated, especially during the very acute phase of small animal models. We have addressed this problem in LPS/D-galactosamine-induced fulminant hepatitis by using sequential micro-MRI scanning. Analysis of T2-weighted MRI signal intensities detected tissue injury in the liver during the early phase (as early as the 3 h timepoint), at which point histological examination revealed only minor morphological changes in hepatic tissues. In the pancreas, increases in the T2-weighted signals were made readily apparent by the pancreatic edema formation that was determined by histological examination. Only minimal pathologies were observed in the renal cortex based on micro-MRI and histological examination. The results of this study have demonstrated the distinct temporal changes that occur in the liver and injured pancreatic acinar cells during the very acute phase of LPS-induced hepatitis.