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Use of a Hanging-weight System for Liver Ischemia in Mice
Published on: August 7, 2012
L-Selectin and chemokine response after liver ischemia and reperfusion
G Martinez-Mier1, L H Toledo-Pereyra, E McDuffie
1Departments of Surgery Research Sciences and Molecular Biology, Borgess Research Institute, Kalamazoo, Michigan 49001, USA.
Background:
L-selectin plays an important role in the early phase of PMNs recruitment in the hepatic microvasculature following liver ischemia and reperfusion (I/R). Leukocyte cytokine chemoattractants (chemokines) cause polymorphonuclear neutrophil (PMN) activation in I/R injury. In this study, we examined the role of L-selectin in the production of chemokines in the liver and lung inflammatory response following 90 min of warm ischemia.
Study Design:
Thirty-six C57BL/6 mice were subjected to partial liver ischemia for a period of 90 min. Three groups of animals were included (n = 12 per group)-sham group, ischemic control, and the ischemic group receiving monoclonal antibody against L-selectin. We evaluated at 3 h: liver injury measurements, serum chemokines (MIP-2 and MIP-1alpha), liver and lung tissue myeloperoxidase (MPO), and liver and lung histology. Statistical analysis included ANOVA, Student-Newman-Keuls', and Kruskal-Wallis multiple comparison Z-value tests.
Results:
The ischemic group treated with anti-L-selectin showed significant decreases in liver enzyme levels and a marked decrease in serum MIP-2 (P < 0.05) when compared to ischemic controls. No reduction in serum MIP-1alpha was noted; however, neutrophil infiltration was significantly ameliorated in the liver and in the lung, as reflected by decreased MPO levels (P < 0.05). Improved histopathological features were observed in the anti-L-selectin-treated group compared to ischemic controls in the liver and the lung.
Conclusions:
Our study suggests an important role for L-selectin in the pathogenesis of liver I/R and the production of chemokines. Anti-L-selectin treatment resulted in improved liver function, decreased neutrophil infiltration, and decreased MIP-2 chemokine response.
Insights
Blocking L-selectin reduces liver injury and inflammation after ischemia. This treatment decreased neutrophil infiltration and MIP-2 chemokine levels, improving liver function.
Area of Science:
- Immunology
- Hepatology
- Inflammation Research
Background:
- L-selectin is crucial for neutrophil recruitment in liver ischemia-reperfusion (I/R) injury.
- Chemokines activate neutrophils, exacerbating I/R-induced damage.
- This study investigates L-selectin's role in chemokine production during liver I/R.
Purpose of the Study:
- To determine the role of L-selectin in liver and lung inflammatory responses following warm ischemia.
- To assess the impact of anti-L-selectin treatment on chemokine production and neutrophil infiltration.
Main Methods:
- C57BL/6 mice underwent 90 minutes of partial liver ischemia.
- Groups included sham, ischemic control, and anti-L-selectin treated mice.
- Evaluated liver injury, serum chemokines (MIP-2, MIP-1alpha), myeloperoxidase (MPO), and histology at 3 hours.
Main Results:
- Anti-L-selectin treatment significantly reduced liver enzymes and serum MIP-2 levels.
- Neutrophil infiltration, indicated by MPO levels, was decreased in both liver and lung.
- Histopathology showed improved tissue integrity in the treated group.
Conclusions:
- L-selectin is implicated in the pathogenesis of liver I/R and chemokine production.
- Anti-L-selectin therapy ameliorates liver injury by reducing neutrophil infiltration and MIP-2 response.
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