Abstract：Objective To explore the mechanism of endoplasmic reticulum stress protein kinase R-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2α(eIF2α) pathway in calcium oxalateinduced renal tubular epithelial cell injury.Methods Human renal tubular epithelial cells HK-2 were divided into control group, calcium oxalate group and calcium oxalate+4-phenylbutyric acid group. The medium was induced by adding calcium oxalate at a final concentration of 5 mmol/L. The calcium oxalate+4-phenylbutyric acid group was added with 4-phenylbutyric acid at a final concentration of 2 mmol/L. CCK-8 method, flow cytometry and DCFH-DA fluorescent probe were used to detect cell viability, apoptosis and intracellular reactive oxygen species(ROS) levels. The expression levels of proteins in the intracellular PERK/eIF2α pathway and downstream Caspase12 and Caspase3 were analyzed.Results OD value of calcium oxalate group(0.42±0.05) was lower than that of control group(0.71±0.08), OD value of calcium oxalate+4phenylbutyric acid group (0.65±0.07) was higher than that of calcium oxalate group (all P<0.05). The apoptosis rate, ROS level, PERK and eIF2α protein levels, Caspase12 and Caspase3 mRNA and protein levels in calcium oxalate group were higher than those in control group, and the differences were statistically significant (all P<0.05). The apoptosis rate, ROS level, PERK and eIF2α protein levels, mRNA and protein levels of Caspase12 and Caspase3 in calcium oxalate+4phenylbutyrate group were lower than those in calcium oxalate group, and the differences were statistically significant (P<0.05).Conclusions Inhibition of endoplasmic reticulum stress with 4-phenylbutyrate in calcium oxalateinduced renal tubular epithelial cell injury can inhibit PERK/eIF2α pathway and alleviate cell apoptosis.
