Objective To observe the expression of angiotensin-converting enzyme( ACE) and ACE2 in rat lung and kidney at different time point after smoke inhalation injury and to explore the possible mechanism. Methods Thirty healthy male SD rats were randomly divided into five groups( n = 6 in each group) , ie. a normal control group, and 4 injury groups of 1 h, 4 h, 10 h and 24 h respectively after 30 min of dense smoke inhalation. The rats were sacrificed at different time point. Lung and kidney tissue samples were collected for measurement of lung wet/dry weight ratio( W/D) , pathological study by HE staining, and ACE and ACE2 expression by immunochemistry staining. Results The inhaled rats all displayed acute lung injury symptoms. The lung W/D in the injury groups were significantly higher compared to the normal control group ( P lt; 0. 05, P lt; 0. 01) . ACE and ACE2 were expressed on cellular membrane of normal lung and kidney. The expression of ACE in lung was increased immediately after injury and the expression of ACE2 in lung was increased at 4 h after injury. No significant changes of the expression of ACE and ACE2 in kidney were observed in the five groups. Conclusion The imbalances of expression of ACE and ACE2 in lung might play an important role in the pathogenesis of smoke inhalation injury.
Objective To investigate the protective effects of ulinastatin on acute lung injury ( ALI)induced by seawater drowning in rats. Methods Thirty male SD rats were randomly divided into three groups, ie. a control group, a model group, and an ulinastatin treatment group. The rats in the model group and the ulinastatin treatment group received intratracheal artificial seawater ( 4 mL/kg) instillation. Then the ulinastatin treatment group received ulinastatin ( 100 000 U/kg) injection after infusion of seawater while the model group received an injection of same amount of saline. The rats were sacrificed at 4 hours after instillation. The pathological changes of lung were evaluated by hematoxylin-eosin stain under light microscope. Lung wet/dry weight ratios were measured to assess the level of pulmonary edema.Concentrations of tumor necrosis factor ( TNF) -α, interleukin ( IL) -1β, IL-6, and IL-10 in bronchoalveolar lavage fluid ( BALF) were detected by enzyme-linked immunosorbent assay ( ELISA) . The myeloperoxidase activity in lung tissue homogenates were measured by colorimetric method. Results Ulinastatin treatmentsignificantly relieved the decline of PaO2 and lung pathological changes, inhibited myeloperoxidase activity,and reduced lung wet/dry weight ratios. Ulinastatin also inhibited the release of TNF-α, IL-1β, and IL-6,whereas increased the expression of IL-10 simultaneously. Conclusion Ulinastatin attenuates seawater induced ALI, which may be related to its inhibitory effects on inflammation reaction through regulating cytokine secretion.