Abstract
The present study investigated the protective effects of lithium borate (LTB) against lung injury secondary to intestinal ischemia/reperfusion (I/R) in rats. Twenty-four male Wistar rats were allocated to four groups: control, I/R, LTB, and I/R+LTB. Intestinal ischemia was induced by superior mesenteric artery occlusion for 45 min, followed by 3 h of reperfusion. The LTB group received 15 mg/kg oral LTB for 5 days; the I/R+LTB group underwent I/R following the same LTB protocol. At the end of the experiment, lung tissue samples were taken from the rats and subjected to biochemical, histopathological, and immunohistochemical analyses. Biochemical results showed an increase in superoxide dismutase (SOD) activity, a reduction in catalase (CAT) and glutathione peroxidase (GSH-Px) activities, a reduction in glutathione (GSH) levels, and an increase in malondialdehyde (MDA) levels in the I/R group. LTB treatment reduced oxidative stress by bringing these parameters to values close to those of the control group. Histopathological examination revealed edema, hemorrhage, thickening of the interalveolar septa, and marked inflammatory cell infiltration in the I/R group, which were substantially attenuated in the I/R+LTB group. Immunohistochemical analyses showed increased Bcl-2 and caspase-3 expression in the I/R group, whereas LTB treatment was associated with reduced caspase-3 expression and modulation of Bcl-2 immunoreactivity. In conclusion, LTB attenuates oxidative stress, reduces histopathological lung damage, and suppresses apoptosis following intestinal I/R injury, suggesting its potential protective role against remote lung injury.