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AIM: To investigate the effect of ginkgo biloba extract (EGb 761) on lung injury induced by intestinal ischemia/ reperfusion (Ⅱ/R). METHODS: The rat model of Ⅱ/R injury was produced by clamping the superior mesenteric artery for 60 min followed by reperfusion for 180 min. The rats were randomly allocated into sham, Ⅱ/R, and EGb +Ⅱ/R groups. In EGb +Ⅱ/R group, EGb 761 (100 mg/kg per day) was given via a gastric tube for 7 consecutive days prior to surgery. Rats in Ⅱ/R and sham groups were treated with equal volumes of the vehicle of EGb 761. Lung injury was assessed by light microscopy, wet-to- dry lung weight ratio (W/D) and pulmonary permeability index (PPI). The levels of malondialdehyde (MDA) and nitrite/nitrate (NO2-/NO3-), as well as the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) were examined. Western blot was used to determine the expression of inducible nitric oxide synthase (iNOS). RESULTS: EGb 761 markedly improved mean arterial pressure and attenuated lung injury, manifested by the improvement of histological changes and significant decreases of pulmonary W/D and PPI (P < 0.05 or 0.01).Moreover, EGb 761 markedly increased SOD activity, reduced MDA levels and MPO activity, and suppressed NO generation accompanied by down-regulation of iNOS expression (P < 0.05 or 0.01). CONCLUSION: The results indicate that EGb 761 has a protective effect on lung injury induced by Ⅱ /R, which may be related to its antioxidant property and suppressions of neutrophil accumulation and iNOS- induced NO generation. EGb 761 seems to be an effective therapeutic agent for critically ill patients with respiratory failure related to Ⅱ/R.
AIM: To investigate the effect of ginkgo biloba extract (EGb 761) on lung injuryinduced by ischemia/reperfusion (II/R). METHODS: The rat model of II/R injury was produced by clamping the superior mesenteric artery for 60 min. Followed by reperfusion for 180 min. The rats were only assigned to sham, II/R, and EGb +II/R groups. In EGb +II/R group, EGb 761 (100 mg/kg per day) was given via a gastric Tube for 7 consecutive days prior to surgery. Rats in II/R and sham groups were treated with equal volumes of the vehicle of EGb 761. Lung injury was assessed by light microscopy, wet-to-dry lung weight ratio (W/D) And the pulmonary permeability index (PPI). The levels of malondialdehyde (MDA) and nitrite/nitrate (NO2-/NO3-), as well as the activities of superoxide dismutase (SOD) and myeloperoxidase (MPO) were examined. Western blot was used To determine the expression of inducible nitric oxide synthase (iNOS). RESULTS: EGb 761 markedly improved mean arterial pressure an d attenuated lung injury, manifested by the improvement of histological changes and significant of of pulmonary W/D and PPI (P < 0.05 or 0.01). Moreover, EGb 761 markedly increased SOD activity, reduced MDA levels and MPO activity, and suppressed NO generation Accompanied by down-regulation of iNOS expression (P < 0.05 or 0.01). CONCLUSION: The results indicate that EGb 761 has a protective effect on lung injury induced by II /R, which may be related to its antioxidant property and suppressions of neutrophil accumulation And iNOS-induced NO generation. EGb 761 seems to be an effective therapeutic agent for critically ill patients with respiratory failure related to II/R.