Advances in perimenstrual asthma / 医学研究生学报

Perimenstrual asthma (PMA) is a manifestation of asthma, occurred in a special physiological period of women. It has clinical manifestations of asthma and its own characteristics. It can be caused by not only general asthma inflammatory mediators, such as leukotrienes, prostaglandins, and abnormal immune factors, but also the change trend of sex hormones in the special period. For example, the balance between the proportion of estradiol and progesterone in the circulation may convert allergic reactions into anti-inflammatory reactions, which reduces eosinophils lung recruitment and increases IL10 production, or estradiol may produce proinflammatory effect, which increases the regeneration of IL4, IL1β, and TNFα, exacerbates allergic pulmonary inflammation, causes and aggravates premenstrual or menstrual asthma. Therefore, the treatment of PMA is also different from that of the general asthma. This article focuses on the understanding of this special type of asthma, and reviews the current situation of its risk factors, pathogenesis, clinical manifestations, treatment plan and other aspects.

AP-1 Decoy modulating MMP-2/TIMP-1 imbalance induced by bleomycin-A5 in pulmonary fibroblasts / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the effect of AP-1 Decoy on matrix metalloproteinase 2 (MMP-2) and tissue inhibitor of metalloproteinase (TIMP-1) imbalance induced by bleomycin-A5 (BLM-A5) in pulmonary fibroblasts.</p><p><b>METHODS</b>Pulmonary fibroblasts were primary cultured, and transferred with AP-1 Decoy before treated with BLM-A5. MMPs activity in medium was determined by gelatin zymography. Protein content of TIMP-1 in medium was detected by ELISA. Expression of MMP-2 mRNA and TIMP-1 mRNA were determined by reverse transcriptase-polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>BLM-A5 induced the increase in activity of MMP-2 at 12 h [A: (0.77 +/- 0.08) vs (0.65 +/- 0.07) P < 0.05], but it was suppressed by AP-1 Decoy [A: (0.68 +/- 0.05)]. BLM-A5 up-regulated the expression of protein and mRNA of TIMP-1 after 12 h, and 24 h [(39.3 +/- 4.3), (46.3 +/- 4.8) ng/ml vs (28.9 +/- 2.7), (31.6 +/- 2.4) ng/ml] and [Absorbance ratio to beta-actin: (0.94 +/- 0.13, 1.08 +/- 0.06) vs (0.76 +/- 0.07, 0.75 +/- 0.08)] (P < 0.05 or P < 0.01) but AP-1 Decoy modulated the up-regulation. All these indexes in AP-1 Decoy group had no significant difference in contrast to the normal group. Mutant AP-1 Decoy had not the same function as AP-1 Decoy on the expression of MMP-2 and TIMP-1 in pulmonary fibroblasts.</p><p><b>CONCLUSION</b>AP-1 Decoy inhibits the increase in MMP-2 activity and the up-regulation of TIMP-1 induced by BLM-A5 in pulmonary fibroblasts.</p>

Dynamic changes of found in inflammatory zone 1 protein and mRNA expression in the lung with experimental pulmonary fibrosis of the rat / 生理学报

To investigate the role of found in inflammatory zone 1 (FIZZ1) protein in the pathogenesis of experimental pulmonary fibrosis, 48 male Sprague-Dawley rats were randomly divided into two groups, the pulmonary fibrosis group and the control group. Rat pulmonary fibrosis was reproduced by an intratracheal injection of bleomycin (5 mg/kg body weight). Normal saline (1 ml/kg body weight) was given intratracheally injection in the control group. There were 24 rats in each group, and 6 animals were separately killed on the 7th, 14th, 21th and 28th day after treated with bleomycin or normal saline. Then the following tests were undertaken: (1) HE and Masson staining of lung section;(2) Determination of lung tissue hydroxyproline (HYP);(3) Immunohistochemical staining of protein of FIZZ1 in the lung;(4) In situ hybridization of FIZZ1 mRNA in the lung. The results showed: (1) There were full of inflammatory cells in the lung, the interval of alveoli enlarged and many alveolar spaces disappeared on the 7th day after treated with bleomycin in the fibrosis group. Collagen began to proliferate after 14 d. The pulmonary fibrosis was stably established on the 28th day, full of green fibers in the Masson staining of lung section. (2) The expression of FIZZ1 protein in the lung increased after 7 d in bleomycin-treated animals (3.013+/-0.326 vs 0.473+/-0.056, P<0.01 vs control), but was slightly decreased on the 14th day (2.124+/-0.197) and expensively decreased on the 21st day (1.760+/-0.105) and the 28th day (0.691+/-0.081). (3) The expression of FIZZ1 mRNA in the lung also increased after 7 d by treated with bleomycin (3.795+/-0.338 vs 0.678+/-0.087, P<0.01 vs control), but decreased on the 14th day (1.276+/-0.104) and further decreased on the 28th day (0.896+/-0.084). The expression of FIZZ1 protein and mRNA in fibrosis group was higher than that in the control group (P<0.05 or P<0.01). The results suggest that FIZZ1 protein and FIZZ1 mRNA are dynamically changed in the lung with experimental pulmonary fibrosis, which may contribute to the pathogenesis of pulmonary fibrosis.