Mechanism Study of Tea Polyphenols Alleviating Aspirin-induced Injury in GES-1 Cells through Activating Nrf2/HO-1 Pathway
OBJECTIVE To investigate the effect of tea polyphenols(TP)on aspirin-induced injury of human gastric epithelial cells GES-1 and its molecular mechanism.METHODS GES-1 cells were treated with aspirin(19.27 mmol·L-1)and different concentrations of tea polyphenols(50,100,200 μmol·L-1)for 24 h.GES-1 cells were randomly divided into control group,aspirin group(19.27 mmol·L-1),aspirin 19.27 mmol·L-1+TP 50 μmnol·L-1 group,aspirin 19.27 mmol·L-1+TP 100 μmol·L-1 group,aspirin 19.27 mmol·L-1+TP200 μmol·L-1 group.Methyl thiazolyl tetrazolium(MTT)was used to detect the survival rate of GES-1 cells.Flow cytometry and TUNEL assay were used to detect apoptosis of GES-1 cells.Dichlorofluorescein diacetate(DCFH-DA)fluorescent probe was used to detect the levels of reactive oxygen species(ROS)of GES-1 cells.Corresponding kits were used to detect the levels of superoxide dismutase(SOD),catalase(CAT)and malondialdehyde(MDA)of GES-1 cells.Western blot was used to detect the expression levels of B-lymphocytoma-2(Bel-2),B-lymphocytoma-2-associated X protein(Bax),nuclear factor E2 related factor 2(Nrf2)and heme monooxygenase 1(HO-1)of GES-1 cells.RESULTS Compared with the control group,the apop-tosis rate,apoptosis index,ROS,MDA levels,nuclear Nrf2/cytoplasmic Nrf2 ratio,Bax,and HO-1 protein expression levels of GES-1 cells in 19.27 mmol·L-1 aspirin group were significantly increased,while the cell survival rate,Bcl-2 protein expression level,SOD and CAT levels were significantly decreased(P＜0.05).Compared with 19.27 mmol·L-1 aspirin group,the apoptosis rate,apoptosis index,ROS,MDA levels and Bax protein expression levels in aspirin 19.27 mmol·L-1+TP(50,100,200 μmol· L-1)groups were significantly decreased,while the cell survival rate,nuclear Nrf2/cytoplasmic Nrf2 ratio,Bcl-2,Nrf2,HO-1 protein expression levels,SOD and CAT levels were significantly increased(P＜0.05).CONCLUSION Tea polyphenols can alleviate aspirin-induced GES-1 cell damage,and the mechanism may be related to the activation of Nrf2/HO-1 antioxidant pathway and the in-hibition of mitochondrial pathway mediated apoptosis.
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