| BackgroundPulmonary fibrosis is the pathological changes and the final outcome of interstitial lung disease caused by various factors, it includes more than 200 diseases. These diseases share common clinical, respiratory pathophysiological and chest X ray features, though each of them has its own characteristics in clinical manifestations and laboratory tests. Pulmonary fibrosis is characterized by progressive dyspnea and diffuse lesions in radiograph. Its pathological changes take the form of gathering of large numbers of fibroblasts, extracellular matrix deposition, and abnormal lung tissue structure damaged by inflammation. Currently, transforming growth factor-β1 is considered as a key and the most direct cytokine in the formation and development of pulmonary fibrosis, which participates in different sectors in the formation of alveolitis and pulmonary fibrosis.Interleukin-8 is a proinflammatory cytokine, high levels of IL-8 plays a role in the start-up and enlarging of lung inflammation through chemotaxis of neutrophils.The inflammation and oxidation induced by IL-8 can damage alveolar epithelial cells, promote alveolar macrophages to release cytokines, stimulate lung fibroblasts proliferation, collagen synthesis,extracellular matrix deposition and angiogenesis and so on in the pathogenesis of pulmonary fibrosis.Glucocorticoid is still the primary means, although there are many kinds of drugs in clinical treatment of pulmonary fibrosis. Treatment of pulmonary fibrosis depends on the pathogenesis revealing, new treatment strategies should be aimed at the various segments of pathogenesis of pulmonary fibrosis.ObjectiveTo investigate the effects of dexamethasone on the dynamic changes of lung tissue pathology, ultrastructure and the levels of TGF-β1 and IL-8 in serum of Pingyangmycin-induced pulmonary fibrosis in rats.Methods105 healthy male Wistar rats were randomly divided into three groups,the control group(n=25), the model group(n=40) and the dexamethasone group(n=40).The rats both the model group and the dexamethasone group were injected with Pingyangmycin(5mg/kg)through tracheofistulization to induce pulmonary fibrosis, the rats of the control group were injected with equivalent physiological saline. After operation, dexamethasone (4mg/kg body weight) was given intraperitoneally to the dexamethasone group rats once a day. Equivalent saline was administered to rats of both the control group and the model group. On the 1st,7th,14th,21st and 28th day, five rats in the control group and eight rats in both of the other two groups were dissected to observe pathological changes of the lung tissues, ultrastructure,and the levels of TGF-β1 and IL-8 in serum were measured by enzyme-linked immunosorbent assay.Results1. The lung histopathology examination results were consistent with the characteristics of rat pulmonary fibrosis model.2. The lung ultrastructures of the model group and the dexamethasone group Changed significantly compared with the control group.3. The concentrations of TGF-β1 and IL-8 in serum were increased and then decreased in both model group and dexamethasone group, and were significantly higher than those of the control group,specially on the 7th day. Levels of TGF-β1 and IL-8 in serum were similar between the model group and the dexamethasone group, and there was no significant difference between them (p>0.05). Conclusion1. TGF-β1 and IL-8 play an important role in the process of alveolitis and the pulmonary fibrosis induced by Pingyangmycin in rats.2. Dexamethasone (4mg/kg body weight) does not reduce the levels of TGF-β1 and IL-8 in serum of Pingyangmycin-induced pulmonary fibrosis in rats, this may be associated with immunocompromised state, which increases the risk of the chance of infection.
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