| BackgroundThe chronic inflammation in the airway, lung parenchyma and pulmonary vascular is themain characteristics of chronic obstructive pulmonary disease (COPD). More and more researchhave shown that, the imbalance between oxidant and antioxidant plays an important role in thepathogenesis of COPD. Oxidants contained in cigarette smoke can cause lung oxidative stressand result in the lipid peroxidation in cells. 4-hydroxynonenal (4-HNE) is one of the spreadhighly active lipid peroxidation products and plays a mediated role in the cell signal transductionand apoptosis induced by oxidant. As an important factor of the inflammatory damage repair inCOPD, transforming growth factorβ1 (TGF-β1) extensively involves in airway inflammation andairway remodeling.ObjectiveTo explore the relationship between oxidative stress and airway remodeling of chronicairway inflammatory disease caused by smoking through researching effects of different durationof smoking on expression of 4-HNE and TGF-β1 in airway epithelial cells of rats.MethodsThirty healthy male Wistar rats (eight weeks old, supplied by Experimental Animal Centerof Shanxi Medical University) are randomly divided into a control group, a short-term smokinggroup and a long-term smoking group, there are ten in each group. Rat smoking device is inaccordance with Xusanlin's self-made smoking device. The duration for short-term smokinggroup is six weeks with six days one week and twice a day (a time A.M a time P.M) with 15cigarettes one time. The duration for long-term smoking group is 12 weeks with 6 days one weekand twice a day. One time is 15 cigarettes. The control group is raised normally to 20 weeks oldwithout smoking. Observe the histopathology change and detect the expressions of 4-HNE andTGF-β1 in airway epithelial cells of rats by using immunohistochemistry.Results1. Histopathology change The alveolar structure of the control group is normal andcontinuous, small bronchial glands have no inflammatory cell infiltration, alveolar wall isintegral. The long-term smoking group and the short-term smoking group exist in varyingdegrees of alveolar wall thinning or rupture, such as alveolar structure disorder, respiratorybronchiole of the existence of cystic dilatation, alveolar structure integration into the wall andinfiltration of a large number of mononuclear cells and lymphocyte, ciliated epithelial broken off, reduction of the number of cilia, the symptoms of long-term smoking group is noticeable.2. The comparison between immunohistochemical results of 4-HNE and TGF-β1 in airwayepithelial cells The protein expression of 4-HNE in bronchial epithelial cells of the long-termsmoking group(0.264±0.022) and the short-term smoking group(0.204±0.017) are higher thanthe control group(0.174±0.017) and the long-term smoking group is higher than the short-termsmoking group, the differences is statistically significant (all P＜0.05). The protein expression ofTGF-β1 of the long-term smoking group(0.247±0.025) and the short-term smokinggroup(0.199±0.021) are higher than the control group(0.175±0.018) and the long-term smokinggroup is higher than the short-term smoking group, the differences is statistically significant (allP＜0.05).3. The correlation between duration of smoking and the expression of 4-HNE and TGF-β1The duration of smoking is positively correlated with the protein expression of 4-HNE(r=0.731,P＜0.01) and it is positively correlated with the protein expression of TGF-β1(r=0.663, P＜0.01).4. The correlation between the protein expression of 4-HNE and TGF-β1 The proteinexpression of TGF-β1 is positively correlated with the expression protein of 4-HNE in airwayepithelial cells of the control ,the short-term smoking group and the long-term smoking group.(r= 0.935, P＜0.01).ConclusioConclusionsSmoking can cause the protein expression of rats airway epithelial cells 4-HNE and TGF-β1increased. The protein expression between 4-HNE and TGF-β1 is positively correlated, with theduration of smoking increasing the level of expression increases. It means oxidative stresscaused by smoking involved in the process of chronic airway inflammation and airwayremodeling. |
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