Expression Of FIZZ1in The Chronic Obstructive Pulmonary Disease Rats And Effection By Administrated Astragaloside IV

ObjectiveTo observe the dynamic expression of FIZZ1and TNF-α in the chronic obstructivepulmonary disease rats, to explore their roles in chronic obstructive pulmonary disease. At thesame time, to research the possible mechanism of Astragaloside IV (AST) in chronicobstructive pulmonary disease treatment.MethodOne hundred and eight healthy SD rats were randomly divided into four groups: thenormal control group (group A) only18, the COPD model group only30(group B, dividedinto COPD model two weeks group, four weeks group, eight weeks group,10in each group),the Astragaloside IV low dose group30only (group C, divided into a low dose of AST twoweeks group, four weeks group, eight weeks group,10in each group), the Astragaloside IVhigh dose group30only (D group, divided into a high dose of AST two weeks group, fourweeks group, eight weeks group,10in each group). The COPD model was established by themethod of combining fumigation and lipopolysaccharide (LPS) intra-tracheal dripping. Andthe rats in the C, D group were administrated the Astragaloside IV by ig (3,9mg respectively)and in A,B group administrated the sodium carboxy methylcellulose in the same way. Theairway and lung tissue morphological changes were observed by normal slice.Immunohistochemistry and RT-PCR were used to measure the level of FIZZ1and TNF alphaprotein and mRNA in the rats′lung tissues.Result1. The pathological changes of lung tissues in the chronic obstructive pulmonary disease rats:The airway walls were in the complete structure, no inflammatory cells infiltrating around, and the alveolar structure form had not seen the destruction in the normal control group.COPD model two weeks of the bronchial wall and airway smooth muscle thickening, airwayepithelial damaged, part of the cilias fall off, there were a lot of inflammatory cells infiltratingsurrounding the airways and alveolar interval. Compared with the model two-weeks group,COPD model four-weeks group of the bronchial wall and airway smooth muscle quitethickened, the lumen relatively narrow, part of the alveolars damaged, fusion, the alveolarspace expansion, there were still inflammatory cells infiltrating. Compared with the modelfour-weeks group, there were the bronchial wall and airway smooth muscle obviously morethickening and more narrow lumen, most of the alveolar damaged, fusion, the alveolar cavityexpansion, the alveolar interval thickening in COPD model eight-weeks group. Afteradministrated the Astragaloside IV, compared with the same period COPD model groups, theairway wall and alveolar damage had reduced, and a high dose group of AST reduced the moreobviously.2. The mRNA expression of FIZZ1and TNF-α and the protein expression level of FIZZ1andTNF-α in the chronic obstructive pulmonary disease rats:The expression of FIZZ1, TNF-α mRNA and protein in the lung tissues was weak in thenormal control group. In the COPD model group, the expression of FIZZ1, TNF-α mRNA andprotein was stronger as the time extension of stimulating, and was significantly higher than thenormal control group (P <0.05). The expression level of FIZZ1, TNF-α mRNA and proteinwas increased in the COPD model two-weeks group, in the four-weeks group the expressionlevels increased further, in comparison, there were significant differences (P <0.05). Theexpression level in the eight-weeks group is more elevated, compared with the surroundinggroup, there was significant difference (P <0.05). After administrated the Astragaloside IV,compared with the same period COPD model groups, the expression level of FIZZ1, TNF-αmRNA and protein was decreased, and there was significant difference (P <0.05), and a highdose group of AST decreased the more obviously.Conclusion1. The expression of FIZZ1and TNF-α is a dynamic changing in the chronic obstructive pulmonary disease. FIZZ1and TNF-α may be involved in the development process of COPD.2. The Astragaloside IV may reduce airway inflammation and remodeling in COPD rats, maythrough declining the expression of FIZZ1and TNF-α. And its effect is a quantity-efficiencycorrelation.