绿茶提取物表没食子儿茶素没食子酸酯对腹膜透析患者腹膜纤维化的防治作用及其机制研究

目的 探讨绿茶提取物表没食子儿茶素没食子酸酯(epigallocatechin gallate,EGCG)对腹膜透析(peritoneal dialysis,PD)患者腹膜纤维化的防治作用及其机制.方法 培养人腹膜间皮细胞(human peritoneal mesothelial cells,HPMCs),分别以0、1...

Effect of epigallocatechin gallate extracted from green tea on peritoneal fibrosis in peritoneal dialysis patients and its mechanism

Objective To investigate the effect and mechanism of epigallocatechin gallate(EGCG) extracted from green tea on peritoneal fibrosis in peritoneal dialysis(PD) patients. Methods Human peritoneal mesothelial cells(HPMCs) were cultured and pretreated with 0, 12.5, 25, 50, 100 μmol/L EGCG respectively. The epithelial-mesenchymal transition(EMT) model was induced by advanced glycation end products(AGEs). Cells without any treatment were taken as control group. MTT method was used to analyze the effect of EGCG on HPMCs proliferation, scratch test was used to analyze the effect of EGCG on HPMCs migration, Western blot method was used to detect the expression level of HPMCs epithelial molecular marker protein(Snail, E-cadherin, CK, ZO-1)and interstitial molecular marker protein(α-SMA, FSP1), and epithelial transmembrane cell resistance meter was used to detect the effect of EGCG on HPMCs transcellular resistance(TER). Results Compared with the control group, the cell viability of EMT model group was significantly increased, the protein expression levels of Snail, E-cadherin, CK and ZO-1 were decreased, the protein expression levels of α-SMA and FSP1 were increased, and the TER value was increased(P<0.05). EGCG can dose-dependently reduce the viability of HPMCs cells, inhibit the migration of HPMCs cells, increase the protein expression levels of Snail, E-cadherin, CK and ZO-1, decrease the protein expression levels of α-SMA and FSP1, and decrease the TER value(P<0.05). Conclusion EGCG can effectively inhibit the proliferation and migration of HPMCs, increase the permeability of HPMCs, inhibit the EMT of HPMCs,and delay the peritoneal fibrosis by up-regulating the expression of epithelial cell molecular marker protein, down-regulating the expression of interstitial cell molecular marker protein, which has clinical application value.