Role Of Sulodexide In Epithelial-Msenchymal Transition Of Alveolar Epithelial Cells

Idiopathic pulmonary fibrosis (IPF) is a disease characterized by fibroblast accumulation, excessive collagen deposition and matrix remodeling which continues to be associated with considerable morbidity and mortality. Now people think the process termed "epithelial-mesenchymal transition"(EMT) may play an important role in fibrogenesis and it has been proved that TGF-β1can induce this process. Nowadays there is compelling evidence that glycosaminoglycans, for example, heparin which are mainly used as anticoagulant can inhibit organ fibrosis. Some researchers found that this kind of medicine may exert their anti fibrotic effect by influencing the activated coagulation cascade. But some people think glycosaminoglycans have their own anti fibrotic effect which is not associated with the haemostatic system, for example, they found that glycosaminoglycans can prevent TGF-β1overexpression in fibrotic tissues. Sulodexide is isolated from porcine intestinal mucosa and comprised of four naturally glycosaminoglycan components. Compared to low-molecular heparin, it has less side effects and can be taken orally. The influence of sulodexide on pulmonary fibrosis has not been studied yet. This study which is based on the culture of human lung epithelial cells A549in vitro used morphology examination, RT-PCR, Immunofluorescence methods to evaluate the effect of Sulodexide on the marker expression in TGF-β1induced EMT process. So it can determine whether it has anti fibrotic activity beyond its anticoagulation effect. The results show the Sulodexide can partially inhibit the morphology changes and decrease the mesenchymal marker expression induced by TGF-β1. This indicate that sulodexide can inhibit the EMT process and it may present a potential novel anti-fibrotic therapeutic approach for the future.