Naringin is one of the natural
flavonoids extracted from many Chinese medicines. It ameliorates endothelial dysfunctions in
atherosclerosis, diabetes, and
cardiovascular diseases through
free radical scavenging and
antioxidant activities. The aim of the present study was to investigate the protective effects of
naringin against pulmonary endothelial permeability in addition to airway
inflammation in
lipopolysaccharide/cigarette
smoke (LPS/CS)-induced
chronic obstructive pulmonary disease (
COPD) mice.The
COPD mice were exposed to LPS twice through intranasal inhalation and then to cigarette
smoke daily for 6 weeks. The mice were orally administrated with
naringin at doses of 40 or 80 mg/kg one hour before cigarette
smoke exposure since the first day of the experiment.
Naringin significantly alleviated pulmonary histopathological injury, and suppressed inflammatory cell infiltration and
cytokine release in bronchoalveolar lavage fluid.
Naringin decreased fluorescence intensity of
Evans Blue in the lung tissues, and elevated the expression levels of tight junctional
proteins. Meanwhile,
naringin decreased neutrophil/lymphocyte/platelet counts and MDA content in blood, and upregulated Aquaporin1 (AQP1) in the lung tissues. However, the effect of
naringin on airway
inflammation and pulmonary endothelial permeability was inhibited in LPS/CS-treatment AQP1 deficiency mice. These results indicated that
naringin attenuated LPS/CS-induced airway inflammatory and pulmonary hyperpermeability via upregulating AQP1 expression.