Ischemic-
reperfusion injury (IRI) triggers an inflammatory response involving neutrophils/macrophages, lymphocytes and endothelial cells.
Galectin-3 is a multi-functional
lectin with a broad range of action such as promotion of neutrophil adhesion, induction of oxidative stress, mastocyte migration and degranulation, and production of pro-inflammatory
cytokines. The aim of this study was evaluate the role of
galectin-3 in the
inflammation triggered by IRI.
Galectin-3 knockout (KO) and wild type (wt) mice were subjected to 45 min of renal pedicle occlusion. Blood and kidney samples were collected at 6, 24, 48 and 120 h. Blood
urea was analyzed enzymatically, while MCP-1,
IL-6 and IL-1beta were studied by real-time PCR.
Reactive oxygen species (ROS) was investigated by flow cytometry. Morphometric analyses were performed at 6, 24, 48 and 120 h after reperfusion.
Urea peaked at 24 h, being significantly lower in knockout animals (wt = 264.4 +/- 85.21 mg/dl vs. gal-3 KO = 123.74 +/- 29.64 mg/dl, P = 0.001).
Galectin-3 knockout animals presented less acute tubular
necrosis and a more prominent tubular regeneration when compared with controls concurrently with lower expression of MCP-1,
IL-6, IL-1beta, less macrophage infiltration and lower ROS production at early time points.
Galectin-3 seems to play a role in renal IRI involving the secretion of macrophage-related
chemokine, pro-inflammatory
cytokines and ROS production.