| Idiopathic pulmonary fibrosis (IPF) is the representative disease of interstitial lung disease(ILD). Its pathologic characters are alveolitis and pulmonary interstitial fibrosis. It has been proved that the initiation position of pulmonary fibrosis (PF) is in the alveolus and the original stage is alveolitis, the important link of alveolitis is to activate of the chemotactic factors. With the chemotactic factors, there are many inflammatory cells recruitment in the alveolus and be activated, thus, cytokine network is activated and cascade reaction is triggered, which induces the lung injury continuously, in the end PF forms. Macrophage inflammatory protein-1α(MIP-1α) and monocyte chemoattractant protein-1(MCP-1) are the members of C-C folk, they play an important role in PF. Many researchers have discovered that MIP-1α,MCP-1 can lead to PF directly or indirectly through recruiting macrophages and CD-8+T lymphocytes into alveolus. Although MIP-1α,MCP-1 have been notified in PF by abroad researchers, little is known about the mechanism and there is no report about them in domestic. It is troublesome to treat PF and there is shot of ideal drug to use. Glucocorticoid is the only certain effective drug to treat PF which has been debated constantly. The research on traditional Chinese medicine to treat PF is rising fast and there is wide prospect of it. The study including:1. By injecting bleomycin into trachea of rats, we established an PF animal model. 2. The extent of alveolitis and fibrosis of PF rats were quantitied by grades. Result showed that alveolitis and fibrosis of PF rats becomes more serious with time prolongation.3. The concentration of plasma MIP-1α,MCP-1 were detected with ELISA method. Results showed that the level of plasma MIP-1α,MCP-1 of BLM group increased significantly with time prolongation compared with non-BLM group and there is positive relationship between MIP-1αand MCP-1 alternation. It indicated that in the process of PF, there are many chemokines released which activate cytokines network, thus PF continuously develops.4. The concentration of collagen I,III and hydroxyproline (HYP) were detected with immunohistochemistry and acid hydrolysis method respectively and their correlation was analyzed. The results showed that in the different stages of the process of PF, the content of collagen I,III were different, collagen III mainly exists in early and light stage while collagen I in late or heavy stage. We also found that there is positive correlation between the content of collagen I and HYP and there is little correlation between collagen III and HYP. It indicates that collagen I and HYP maybe the mark of PF.5. The mark of PF in PNS group and metrisone group decreased significantly than those in BLM group and the mark of PNS group is the lowest.To sum up, we successfully established rat PF animal model. The alteration regularity of MIP-1α, MCP-1 and other mark of PF, their inner relationships and effects on the process of PF were explored. The results showed that :The levels of plasma MIP-1αand MCP-1 of BLM-induced PF rats increased in the early stage of PF and they paralleled with the state of PF.1. The levels of plasma MIP-1αand MCP-1 are also in line with other mark of PF, such as collagen I, III and HYP. It infers that MIP-1αand MCP-1 may play an important role in PF and probably become the earlier sensitive mark of evaluating the stages of the progress of PF.2. The mark of PF in PNS group and metrisone group decreased significantly than those in BLM group and it indicated that PNS and metrisone can restrain the lung tissue to be fibrotic. We suspect that the probable mechanism were to limit the inflammatory cells leak out and anti-synthetic fiber, so the process of PF was delayed. There were little differences between PNS and metrisone in anti-synthetic fiber. Because of its little side effects, PNS may become an ideal anti-PF medicine.
|
PDF Full Text Request