The Effect Of Erythromycin On Expression Of ILK、e-cad、α-SMA In Rat With Pulmonary Fibrosis Caused By Blemycin

【Objective】 To discuss the expression of ILK、 E-cad、 α-SMA inbleomycin-induced pulmonary fibrosis and the effect of Erythromycin on them.【Methods】90healthy male SD rats were randomly divided into six groups,Group1: normal control group; Group2: model group; Group3: continuous feeding oferythromycin three days before the BLM modeling, and then to BLM modeling, notto be drug intervention; Group4: after BLM modeling2hours,continuous feedingerythromycin for14days; Group5: after BLM modeling14days feedingerythromycin, until the28days; Group6: three days before BLM modeling, beginfeeding erythromycin until the28days.2to6groups rats intratracheal fed bleomycin(5mg/g) to create the animal models of pulmonary fibrosis, group1intratracheal fedan equal volume of saline, the model groups were administered by program.15ratseach group, respectively,7,14,28days were random sacrificed5rats.Let left lungtissue place in4%formaldehyde fixed, then, HE staining and immunohistochemicaldetection of ILK, E-cadherin, α-SMA protein expression; Let the right lung tissue,hydroxyproline detection and RT-PCR, ILKmRNA, E-cadherin mRNA, α-SMAmRNA expression.【Results】1. HE staining showed: Group2organization was mainly inflammatoryresponse,,showing that lung fibroblasts at7d, a large number of inflammatory cellsinfiltration, most of them were lung fibroblasts at14d; a large number of lungfibroblast cells, indicating the formation of pulmonary fibrosis at28d.2to6groupspathological changes similar trend, and gradually to the development of pulmonaryfibrosis, but fibrosis lightest in Group6.2. HYP content: compared with the control group at7d,14d,28d,2-6group levelswere increased, and P <0.05, group2increased to the most obvious; the HYP detection of3,5Group were no significant change compared with Group2;4、6groupwere treated with erythromycin, the contents were decreased, and P <0.05,Group6is the most significant at28d,P <0.01.3. RT-PCR、Immunohistochemistry showed：In the normal lung tissue, ILK, α-SMAwere lowly expressed，E-cad was highly expressed。When pulmonary fibrosis occurs,compared with normal tissue, ILK、α-SMA expression were increased (P <0.05),E-cad expression was decreased (P <0.05); To drugs after the intervention, comparedwith model, ILK, α-SMA expression of4,6group were decreased, E-cad wasincreased (P <0.05), the28days of Group6is the most significant.(P <0.01).【Conclussions】1. Erythromycin can prevent pulmonary fibrosis that induced by bleomycin in rats andthe effect was related to the early medication and treatment..2.The erythromycin can prevent pulmonary fibrosis,and the mechanism may berelated to inhibition of ILK, α-SMA expression, increased levels of E-cad, delayingthe development of the EMT.