| Chronic obstructive pulmonary disease (COPD) is associated with chronic airways inflammation. Many kinds of cytokines and chemokines participate and play a key role in this pathophysiological process. Peroxisome proliferator activated receptors (PPARs) are members of a nuclear hormone receptor/transcription factor superfamily. The transcription factor PPAR forms a heterodimeric complex with the retinoid X receptor, and the complex of PPAR and RXR binds to specific DNA recognition sites and regulates transcriptional events. Recently, PPAR-γhas been shown to play an important role in the control of inflammatory responses, including within the lung, acting on both immune and other cells. Rosiglitazone, as a high selective PPAR-γligand, activates PPAR-γwhen binding to it and inhibits many inflammatory responses. While all-trans retinoic acid (ATRA) exhibits a wide spectrum of activities, including anti-inflammatory properties. This study was mainly conducted to investigate the influence of rosiglitazone and ATRA on the expression of chemokines in a rat model of COPD and their possible mechanisms, and the specific process is as fowllowing: In our study 48 Sprague-Dawley rats were randomed equally divided into four groups, (1) Control group: without any disposal. (2) COPD group:Adult rats were administered with LPS by intratracheal instillation and smoked. (3) Rosiglitazone group(RGZ group): rats were administered with rosiglitazone 0.02mg by means of gavage besides everyday smoking and LPS instillation. (4) ATRA group: rats were administered with ATRA 15mg/kg by means of gavage besides everyday smoking and LPS instillation. After 29 days all the rats were killed and lung tissues were kept for study. Using the Image-Pro plus analysis software to analyze the lung alveolar number(MAN) and lung alveolar diameter(MAD), and to assess the histological changes of lung tissues; Measuring MIP-2 level in the lung tissue homogenates and bronchoalveolar lavage alveolar macrophage cell culture by means of ELISA;The expressing level of CINC-1 mRNA in the lung tissues was determined by RT-PCR; at the same time the lung myoloperoxidase (MPO) level was measured. Finally all the data were processed in SPSS software, and the main results are as following: 1. The histological results: In COPD group, inflammatory cells scattered in the bronchioli and alveoli, and alevolar walls were severely destroyed; In RGZ group and ATRA group, a lesser inflammation and damage in the lung contrasted with COPD group. The lung MAN in COPD group was lower than control group (P<0.01); The MAN in RGZ group and ATRA group were higher than COPD group (P<0.05) but lower than control group (P<0.01). The lung MAD in COPD group(23.84±5.00μm)was higher than control group (7.18±0.61μm,P<0.01); The MAD in RGZ group(11.44±1.88μm) was lower than COPD group(P<0.05) and had no statistical difference with control group; The MAD in ATRA group(12.90±1.73μm)was lower than COPD group(P<0.05),but higher than control group(P<0.05). 2. The level of lung MIP-2(41.43±7.36 pg/ml) in COPD group was higher than control group(7.05±3.92 pg/ml,P<0.01); MIP-2 level(15.12±6.60pg/ml)in RGZ group was lower than COPD group(P<0.05) and had no statistical difference with control group; MIP-2 level ( 16.62 ±6.03pg/ml)in ATRA group was lower than COPD group(P<0.05) andhigher than control group(P<0.05); MPO level in COPD group(12.20±1.72 U/g) was higher than control group(7.97±0.76U/g, P<0.01).MPO content in RGZ group(8.34±1.88 U/g)and ATRA group(9.13±2.15U/g)were both lower than COPD group(P<0.05) and had no statistical difference with control group. 3. The alveolar macrophage cell culture MIP-2 content(328.2±9.5 pg/ml) in LPS group was higher than control group(11.1±2.2 pg/ml,P<0.01), the corresponding MIP-2 in RGZ group(133.9±2.2 pg/ml)and ATRA group(107.2±2.2 pg/ml) was lower than LPS group(P<0.05) but higher than control group(P<0.05). 4. The expressing level of lung CINC-1mRNA in COPD group was higher than control group(P<0.01); the CINC-1mRNA level in Rosiglita...
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