| Objective: To investigate the effect of mesenchymal stem cells on the expression of matrixmetalloproteinase-2（MMP-2）and tissue inhibitor of metalloproteinase-1（TIMP-1）inpulmonary fibrosis rats and explore its intervention mechanism of action.Methods: The BMSCS of4-week-old SD rat were isolated, cultivated and purified in vitro.Forty-eight SD rats were randomly divided into four groups：normal control group; BLMgroup; BLM＋MSCs group; BLM14d＋MSCs group. The pulmonary fibrosis was madeby intratracheal injection of bleomycin(5mg/kg).The normal controls received intratrachealinjection a same amount of normal saline（NS）instead of bleomycin. MSCs(1×106) wereinjected into the caudal vein immediately or14days after challenge with bleomycinrespectively. The rats were sacrificed on28day. The pathological changes were observedby HE and Masson staining methods. The expressions of TGF-β1, MMP-2and TIMP-1were detected by Western blot.Results:①MSCS were successfully cultured and identified.②Alveolitis and pulmonaryfibrosis in model group were remarkably aggravated compared with those in normal controlgroup. Alveolitis and pulmonary fibrosis in BLM＋MSCs group were significantlyalleviated compared with those in model group. There was no significant differencebetween BLM14d＋MSCs group and model group for alveolitis and pulmonary fibrosis. ③The expression of TGF-β1and TIMP-1in model group were significantly increasedcompared with those in normal control group. For rats received MSCs after bleomycinadministration（both BLM＋MSCs group and BLM14d＋MSCs group）, the expressionsof TGF-β1and TIMP-1were significantly decreased as compared with rats received noMSCs. For the expression of MMP-2, there was no significant difference among groups.Conclusion：MSCS can effectively prevent the development of pulmonary fibrosis,especially in the early stage, which might be related to the reduction of TGF-β1and theregulation of MMP-2and TIMP-1balance. |
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