Objective To observe barrier function changes of gut mucosa in rats with acute respiratory distress syndrome(ARDS)．Methods Forty SD rats were randomized to an experiment group (n：30)and a control group(n=10)．Oleic acid was injected via vena femoralis to establish ARDS ratmode1．Subgroups in the experiment group were randomly divided by time 30 min，2 h，4 h interval after injection(n=10 in each subgroup)．Concentration of D-lactate and endotoxin and activity of diamineoxidase in blood plasma were measured．Histopathological changes of small intestine were observed under light microscope．Results Compared with the control group，the activation of diamine oxidase in the experiment group was higher after 30 min of injection(Plt;0.01)．Concentration of D-lactate，the activity ofdiamine oxidase and endotoxin level in the experiment group were all elevated after 2 hours of injection(all Plt;0.05)，and further elevated after 4 hours．In the rats’villous interstitial after 2 hours of the injection，there were edema，hyperemia，and infiltration of neutrophils，eosinophils and lymphocytes．After 4 hours ofthe injection，the villous epithelium showed desquamation，necrosis，denaturalization and erosion，associated with infihration of lymphocytes and neutrophils in the mucosa．Conclusion In oleic acid-induced ARDS．permeability of gut mueosa increases and gut barrier is dysfunctional．
Objective To study the effect of tumor necrosis factor-α( TNF-α) onhypermetabolism of skeletal muscle protein in rats with chronic obstructive pulmonary disease ( COPD) and explore its underlying mechanism. Methods Forty-five SD rats were randomly divided into a normal control group, a COPD group and a COPD + TNF-α group, with 15 rats in each group. COPD model was established by passive cigarette smoking in COPD group and COPD + TNF-αgroup. Then the extensor digitorium longus muscles ( EDL) were dissected and incubated in vitro muscle incubation system with adequate oxygen supply. The EDL were either cultured with or without recombinant rat TNF-α( 10 μg/L) . The mRNA and protein expressions of proteasome subunit C2 in EDL were quantified by real-time quantitative PCR and Western blot analysis, respectively. Results The mRNA and protein expressions of proteasome subunit C2 were both significant higher in the COPD group and COPD + TNF-αgroup than those in the normal control group( P lt;0. 01 or 0. 05) . The COPD+TNF-αgroup had higher expression of proteasome subunit C2 mRNA than that in the COPD group( P lt; 0. 01) , whereas the protein expression was not significantly different( P gt; 0. 05) . Conclusion Incresed proteolytic metabolism in skeletal muscle in COPD might be regulated by TNF-αactivated ubiquitin-dependent pathway.
Objective To study the role of ubiquitin-proteasome pathway in diaphragm of COPD rats. Mathods Thirty rats were divided into a normal control group and a COPD group. COPD model was established by exposure to cigarette smoke for three months. The protein levels of E2-14k and proteasome subunit C8 in diaphragms were measured by Western blot. The mRNA levels of ubiquitin and proteasome subunit C2 in diaphragms were measured bymeans of realtime polymerase chain reaction( RT-PCR) . Results Compared with the control group, the protein expression of E2-14k increased significantly in the COPD group ( 0. 81 ±0. 28 vs 0. 50 ±0. 25, P lt;0. 05) , but C8 protein level was not significantly different between the two groups( P gt;0. 05) . The mRNA expression of ubiquitin increased significantly in the COPD group( 0. 89 ±0. 20 vs 0. 50 ±0. 15, P lt;0. 05) , but C2 mRNA level was not significantly different between the two groups ( P gt; 0. 05 ) . Conclusions The mRNA and protein expressions of ubiquitin-proteasome pathway in diaphragmincreased significantly in COPD rats, suggesting that the activity of ubiquitin-proteasome pathwayincreased, which lead to an increase of protein degradation.
Objective To investigate the role of AKT/FOXOs /atrogin-1/MuRF1 signaling pathway in skeletal muscle atrophy in rats with chronic obstructive pulmonary diseases( COPD) .Methods Passive cigarette smoking was used to establish COPD model. The protein expression of atrogin-1, MuRF1, FOXO-1, phosohorylated-AKT and total AKT were measured by Western blot. The mRNA expression of atrogin-1, MuRF1 and FOXO-1 were measured by reverse transcription-polymerase chain reaction( RT-PCR) . Results Compared with the control group, the mRNA expressions of atrogin-1, MuRF1 and FOXO-1 significantly increased in extensor digitorum longus ( EDL) of the COPD group (Plt;0.05 ) . Meanwhile the protein expression of atrogin-1 and MuRF1 significantly increased in the COPD group(Plt;0.05) , while the protein expression of FOXO-1 was not significantly different between two groups(Pgt;0.05) . In addition, , the protein expression of phosohorylated-AKTand the ratio of phosohorylated-AKT to total AKT significantly increased in EDL of the COPD group(Plt;0.05) . Conclusion The mRNA and protein expression of AKT/FOXOs/ atrogin-1 /MuRF1 in skeletal muscle are significantly increased in COPD rats, suggesting that AKT/FOXOs/ atrogin-1 /MuRF1 signalling pathway plays a crucial role in skeletal muscle atrophy of COPD.
ObjectiveTo summarize the clinical manifestations, diagnosis and treatments of chronic eosinophilic pneumonia (CEP).MethodsThe clinical and pathological data of five patients with CEP diagnosed in this hospital between January 2011 and January 2015 were retrospectively analyzed.ResultsThere were five CEP cases including two males and three females, and one case with allergic rhinitis, two cases with bronchial asthma, two cases with allergic history, and one case with allergic skin rash. The main clinical manifestations were fever, cough, expectoration, shortness of breath and chest pain, and often accompanied by fatigue, anorexia and weight loss. The main signs included moist rales, scattered wheeze and crackles. There were significantly increased peripheral blood eosinophils count, the proportion of eosinophils, and the proportion of eosinophils in bronchoalveolar lavage fluid in all five cases. The main imaging features were airway infiltration, real change shadow and ground glass shadow. All of five cases were treated with glucocorticoid, and one of them relapsed during follow-up.ConclusionsThe onset of CEP is insidious. The clinical manifestations of CEP are lack of specificity, and often associate with asthma and allergic dermatitis. Eosinophils significantly increase in peripheral blood and bronchoalveolar lavage fluid in most of CEP patients. The typical image is peripheral and subpleural distribution of lung infiltrates.