| Objective :Human peritoneal mesothelial (HPMCs)cells are important components of the peritoneum and they play a very important role in peritoneal dialysis and peritoneal fibrosis caused by peritoneal dialysis(PD). The physiomorphological alteration of PD related peritoneal fibrosis is marked by the loss of peritoneal mesothelial cell layer and the accumulation of extracellular matrix (ECM). And during the two processes, HPMCs are not only passive sufferers, but also active participants. In the incompatible physiological environment induced by the peritoneal dialysate, HPMCs are injured and their proliferations are suppressed. They also secret ECM and ECM accumulating cytokines including the most important cytokine among them: transforming growth factor- ?1 (TGF- ?1).Studies show that glucose of high concentration and its metabolic products are the main factors of physiological incompatibility of peritoneal dialysate, which cause the above damages to HPMCs. Glucose of high concentration can destroy the intercellular junctions among HPMCs and make them disconnected. At the same time, it can up-regulate the expression of p21, c-myc and bax, and down-regulate the expression of bcl-2. As will lead to apoptosis. Glucose of high concentration promotes the synthesis of TGF-?1 in HPMCs, which is an important regulating factor in the initiation and development of fibrosis. The mechanism of TGF-?1 in the accumulation of ECM is mediated by disequilibrium between MMP and TIMP with the down-regulation of matrix metalloproteinases (MMPs) and the up-regulation of tissue inhibitor of metalloproteinase (TIMP). Fibronectin (FN) is an important component of ECM, which forms the scaffold for the other components of ECM. It also plays an important role in fibrosis.Interferon-α(IFN-α), which has various biological activities, has been clinically used in the prevention and cure of hepatocirrhosis, idiopathic pulmonary interstitial fibrosis. Experiments have confirmed that the antifibrotic mechanism of IFN-αis mediated by the activation of MMP-2 and the inhibition of TGF-?1. But until now, there still have not correlative investigations on the prevention of peritoneal fibrosis of IFN-α. In this study, we investigated the effect of IFN-αon the secretion of FN,TGF-?1,MMP-2 in HPMCs under the condition of glucose of high concentration trying to understand the significance of IFN-αon the prevention and cure of peritoneal fibrosis.Method: HPMCs were isolated from discarded peritoneal dialysate and primarily cultured .The secondarily cultured HPMCs were used in the experiment. We can make cellular evaluation based on observation of the cells by light microscope and based on staining of immuno-histochemical with antibody for vimentin,cytokeratin8,factor Ⅷ. HPMCs were divided into experimental groups and control group. The experimental groups were treated with 2.5%glucose and IFN-αof different concentrations. The supernate was collected after 24h, 48h and 72h to detect FN,TGF-?1,MMP-2 in it.Result: 1. HPMCs: The cultured HPMCs were spindly at first. About a week later, they connected with each other and took on a slabstone-like appearance. Immunohistochemistry analysis showed positive immunoreactivity of vimentin and cytokeratin and negative immunoreactivity of factor Ⅷ in these cells. 2.FN: The FN-like immunoreactivity in all the experimental groups treated with 2.5% glucose was significantly higher than that in the control group (p<0.05). The FN-like immunoreactivity in groups treated with 2.5% glucose and IFN-αwas significantly lower than that in groups treated with 2.5% glucose only(p<0.05); IFN-α reduced the synthesis of FN in a dose-dependent manner. 3. TGF-?1: The TGF-?1 -like immunoreactivity in groups treated with 2.5% glucose was significantly higher than that in the control group (p<0.05). The TGF-?1 -like immunoreactivity in groups treated with 2.5% glucose and IFN-αwas significantly lower than that in groups treated with 2.5% glucose only(p<0.05);IFN-αreduced the synthesis of TGF-?1 in a dose-dependent...
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