| Background: The chronic obstructive pulmonary disease (COPD) is disease which one kind may prevent may treat, has outside certain remarkable lungs the effect, possible and the patient individual order of severity concerns. Lungs characteristic performance for airflow limitation is not fully reversible, often becomes carries on the development, concerns with the lungs to the noxious gas or the pellet unusual response. Because COPD its sick population are many, the mortality rate is high, and the social economy bears heavily, has become an important public health question, is the severely impair humanity health important chronic respiratory disorder. Its pathogenesis is very complex, take the neutral granular cell as the main effects cell's gas channel inflammation response is one of its morbidity main mechanisms, the gas channel inflammation involves many kinds of inflammatory cells and the cell factor, the tumor necrosis factor-α(TNF-α), the interleukin-8 (IL-8), the transforming growth factor-β1 (TGF-β1) and so on cell factors to have the influential role in the lungs gas channel inflammation. Prostaglandin E1 (PGE1) is one kind of the prostaglandin,on clinical mainly uses in improving the microcycle function, recent years discovered that PGE1 may through suppress TNF-α, TGF-β1 and so on factor expressions to oppress the anti-acute lung damage, the lung fibrosis and the bronchial tube asthma's airflow inflammation responded, but has not seen the related report to the COPD airflow inflammation's influence. This topic through observes the influence of PGE1 to the COPD rats airflow in TNF-αand TGF-β1 and artery blood gas and so on, provides the experiment basis for PGE1 treats COPD to apply in clinical ,and provides the new mentality of the COPD treatment.Objective: Observes influences of PGE1 to the COPD rats artery blood gas, the lung tissue pathological changes, the inflammatory cell counting and the classification in BALF, as well as the expression of TNF-αand TGF-β1 in lung tissue, discusses the intervention function of PGE1 to the COPD rats airflow inflammation and the possible mechanism.Method: Thirty Wistar rats were randomly divided into three groups, the control, model and treatment groups. The models of COPD were established by intratrachel instillation of lipopolysaccharide (LPS) and daily exposure to cigarette smog. From the second to 28th days, except the 15th days, put the 2ml Lipo- Prostaglandin E1 (PGE1) dissolved into the 8ml normal saline, the rats in treatment group were given by i. v. at a dose of 0.25 ml·(0.1kg)-1 from vena candalis before smog exposure. 28 days later, assay the rats artery blood gas, then killed them, total and differential cell counts in bronchoalveolar lavage fluid (BALF) were observed, and the pathomorphological changes in the lung were analyzed. The expression of transforming growth factor-β1 (TGF-β1) on the lung tissue were detected by immunohistochemical method. The expressions of tumor necrosis factor-α(TNF-α) in the BALF were evaluated by ELISA. The expressions of TGF-β1mRNA and TNF-αmRNA of lung tissue were detected by RT-PCR.Result: 1.According to the rats artery blood gas analysis and the rats lung tissue pathology can determine that the pathology change in COPD rats model conforms to the human COPD characteristic. 2. the artery blood oxygen pressure and the artery blood oxygen saturation in treatment group (88.36±2.26) mmHg, (84.19±1.82) % has the distinct improvement compare the model group (75.66±3.74) mmHg, (77.68±2.89) %,the difference has statistics significance (P<0.05). 3. Pathologic changes of the lung tissue of treatment group were better than that of the model group while worse than the control group. 4. The white blood cell total and the neutral granular cell number in BALF in the treatment group (5.655±2.131, 0.819±0.310)×106/L were lower than the model (10.556±2.996, 2.417±0.687)×106/L, the difference have statistics significance (P<0.05). 5. The TNF-αcontent in lung tissue in treatment group (730.750±53.758) pg/ml were lower than the model (930.700±65.221) pg/ml, the difference has statistics significance (P<0.05), but was still higher than the control group (331.000±77.084) pg/ml, the difference has statistics significance (P<0.01). 6. The lung tissue TGF-β1 expression scoring in the treatment group (2.250±1.165) were lower than the model group (5.900±1.370), the difference has statistics significance (P<0.05), but is higher than the control group (0.700±0.823), the difference has statistics significance (P<0.01). 7. The lung tissue TNF-αmRNA, TGF-β1 mRNA expression in treatment group (1.095±0.207, 0.781±0.200) were lower than the model group (1.448±0.266, 1.063±0.202), the difference has statistics significance(P<0.05), but was still higher than the control group (0.723±0.137, 0.365±0.087), the difference has statistics significance (P<0.01).Conclusion: Intratrachel instillation of lipopolysaccharide (LPS) twice and daily exposure to cigarette smog to establish the models of COPD rats were successful; It conforms to the development pathology physiology condition of human COPD; Arterial blood gas analysis and lung histopathology to determine the joint observation can be used as a rat model of COPD model of success. PGE1 may improve the level of COPD rats the artery blood oxygen pressure and the artery blood oxygen saturation obviously, reduces the pulmonary emphysema change; TNF-αand TGF-β1 increases obviously in the COPD rats airflow tissue's expression; Prostaglandin E1 can reduce the inflammatory cell total and the neutral granular cell number in BALF, reduces the TNF-αcontent in BALF and the lung tissue TGF-β1 expression, reduce the level in the lung tissue TNF-αmRNA and TGF-β1mRNA expression, thus has certain prevention and control effect to the COPD rats airflow inflammation. |
PDF Full Text Request