TY  - JOUR
A1  - Czerny, Christoph
A1  - Kholmukhamedov, Andaleb
A1  - Theruvath, Tom Prakash
A1  - Maldonado, Eduardo N.
A1  - Ramshesh, Venkat K.
A1  - Lehnert, Mark
A1  - Marzi, Ingo
A1  - Zhong, Zhi
A1  - Lemasters, John J.
T1  - Minocycline decreases liver injury after hemorrhagic shock and resuscitation in mice
T2  - HPB surgery
N2  - Patients that survive hemorrhage and resuscitation (H/R) may develop a systemic inflammatory response syndrome (SIRS) that leads to dysfunction of vital organs (multiple organ dysfunction syndrome, MODS). SIRS and MODS may involve mitochondrial dysfunction. Under pentobarbital anesthesia, C57BL6 mice were hemorrhaged to 30 mm Hg for 3 h and then resuscitated with shed blood plus half the volume of lactated Ringer’s solution containing minocycline, tetracycline (both 10 mg/kg body weight) or vehicle. Serum alanine aminotransferase (ALT), necrosis, apoptosis and oxidative stress were assessed 6 h after resuscitation. Mitochondrial polarization was assessed by intravital microscopy. After H/R with vehicle or tetracycline, ALT increased to 4538 U/L and 3999 U/L, respectively, which minocycline decreased to 1763 U/L (P<0.01). Necrosis and TUNEL also decreased from 24.5% and 17.7 cells/field, respectively, after vehicle to 8.3% and 8.7 cells/field after minocycline. Tetracycline failed to decrease necrosis (23.3%) but decreased apoptosis to 9 cells/field (P<0.05). Minocycline and tetracycline also decreased caspase-3 activity in liver homogenates. Minocycline but not tetracycline decreased lipid peroxidation after resuscitation by 70% (P<0.05). Intravital microscopy showed that minocycline preserved mitochondrial polarization after H/R (P<0.05). In conclusion, minocycline decreases liver injury and oxidative stress after H/R by preventing mitochondrial dysfunction.
Y1  - 2012
UR  - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/22798
UR  - https://nbn-resolving.org/urn:nbn:de:hebis:30:3-227989
SN  - 1607-8462
SN  - 0894-8569
N1  - Copyright © 2012 Christoph Czerny et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
VL  - 2012
IS  - Art. 259512
SP  - 1
EP  - 9
PB  - Hindawi
CY  - New York, NY
ER  -