Abstract

Objective To investigate the variation and potential function of pre-B cell colony enhancing factor (PBEF) in obesity rats with acute respiratory distress syndrome (ARDS). Methods Forty healthy male Sprague-Dawley (SD) rats were randomly divided into control group, obesity group, ARDS group, and obesity ARDS group, with 10 rats in each group. Rats in the two obesity groups were fed with high-fat diet, and the rats in other groups were fed with normal fodder. After successful obesity models were reproduced as the mean weight of rats in obesity model groups was up over 20% compared to other groups, the rats in two ARDS groups were injected with lipopolysaccharide (LPS) through tail vein to reproduce ARDS models, and the rats in other groups were injected with the same volume of saline. The lung tissues were harvested at 8 hours after ARDS model reproduction to determine lung dry/wet weight (D/W) ratio; real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the expression of PBEF mRNA, and the proteins expressions of PBEF and nuclear factor-κB p50 (NF-κB p50) were detected by Western Blot; the distribution and expression of PBEF was also examined by immunohistochemical staining. Pathological changes of lung tissues were observed after hematoxylin-eosin (HE) staining. Results Obesity rat models were set up successfully with 6 weeks of high fat diet. The D/W ratio of rats in obesity, ARDS, and obesity ARDS groups was significantly lower than that of control group (0.195±0.005, 0.179±0.003, 0.153±0.011 vs. 0.224±0.007, all P < 0.05), and D/W ratio in obesity ARDS group was significantly lower than that of ARDS group, indicating that the lung water content of ARDS rats and non ARDS rats could be influenced by obesity. In obesity group, ARDS group and obesity ARDS group, the expression of PBEF mRNA in lung tissues was increased in turn [it was (1.77±0.22), (3.29±0.14), (5.52±0.14) folds of that in control group respectively, all P < 0.01], and the proteins expression of PBEF and NF-κB p50 in lung tissues were also increased in turn [PBEF protein was (1.75±0.16), (2.71±0.19), (3.83±0.18) folds of that of control group, and NF-κB p50 protein was (1.56±0.12), (1.95±0.12), (2.48±0.24) folds of that of control group respectively, all P < 0.01], and there were significant differences between any two groups. There was almost no PBEF expression in lung tissues of control group detected by immunohistochemical staining, and a little PBEF expression in obesity group, the obvious increased PBEF expression was found in ARDS group, as well as PBEF expressed strikingly in alveolar walls exudates and alveolar spaces exudates of obesity ARDS group. It was shown by HE staining there were no significant pathological changes in lung tissue of rats in the control group; a few inflammatory cells infiltrated in lung tissue of obesity group, thicken alveoli septum and a number of the red cells infiltrated in alveolar spaces were found in ARDS group; the inflammation degree in lung tissue is most serious, a huge amount of exudates, red cells and inflammatory cells in alveolar spaces were found in the obesity ARDS group. Conclusions PBEF might be involved in the process of the development of ARDS in obese rats through the regulation of activity of NF-κB. Key words: Obesity; Acute respiratory distress syndrome; Pre-B cell colony enhancing factor; Nuclear factor-κB

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