Gadolinium chloride (GdCl3), a Kupffer cells inhibitor, attenuates
acute lung injury; however, the mechanisms behind this effect are not completely elucidated. We tested the hypothesis that GdCl3 acts through the inhibition of lung parenchymal cellular apoptosis. Two groups of rats were injected intraperitoneally with saline or E. coli
lipopolysaccharide. In two additional groups, rats were injected with GdCl3 24 hrs prior to saline or LPS administration. At 12 hrs,
lung injury,
inflammation, and apoptosis were studied. Lung water content,
myeloperoxidase activity, pulmonary apoptosis and
mRNA levels of
interleukin-1 β , -2, -5, -6, -10 and TNF- α rose significantly in LPS-injected animals. Pretreatment with GdCl3 significantly reduced LPS-induced elevation of pulmonary water content,
myeloperoxidase activity, cleaved
caspase-3 intensity, and attenuated pulmonary TUNEL-positive cells. GdCl3 pre-treatment upregulated
IL-1 β , -2 and -10 pulmonary gene expression without significantly affecting the others. These results suggest that GdCl3 attenuates
acute lung injury through its effects on pulmonary parenchymal apoptosis.