Hesperidin is a naturally common
flavonoid. It is an abundant and cheap by-product of citrus cultivation. It is reported to have antioxidative, anti-inflammatory and
anticarcinogenic effects. This work was performed to investigate the possible protective role of
hesperidin in ameliorating the effect of experimentally induced intestinal
ischemia/reperfusion injury (I/R) on lung tissue, histologically, immunohistochemically and biochemically. Thirty male Wistar adult albino rats were randomized into three groups named: group I (control group); group II (I/R); and group III (I/R with
hesperidin). Intestinal I/R was induced by occluding the superior mesenteric artery for 60 min, followed by 120 min of reperfusion period. Animals were given
hesperidin orally 1h before the onset of
ischemia. At the end of the reperfusion period the lung tissues were extracted for histopathological examination and immunohistochemical detection of the distribution of
inducible nitric oxide synthase (iNOS).
Pulmonary edema was evaluated by lung tissue wet/dry weight ratios. The levels of
malondialdehyde (MDA, a
biomarker of oxidative damage),
myeloperoxidase (MPO, an index of the degree of neutrophil accumulation) and
glutathione (GSH, a
biomarker of protective oxidative injury) were also determined in all dissected tissues. Pretreatment with
hesperidin (in group III) alleviated lung morphological changes noticed in I/R group and the levels of MDA and MPO were significantly decreased whereas those of GSH were significantly increased. Immunohistochemical study revealed a significant decrease in the iNOS.
Hesperidin also significantly alleviated the formation of
pulmonary edema as evidenced by the decreased organ wet/dry weight ratios.
Hesperidin exerts a protective effect against lung damage induced by intestinal I/R injury in rats by reducing oxidative stress.