Study On Hydroxycitrate Inhibiting Hyperoxalate-induced Renal Tubular Epithelial Cells Injury

Objective:To explore the inhibitory effect of hydroxycitrate(HCA)on hyperoxalate-induced renal tubular epithelial cells injury.Methods:NRX-52E cells was divided into control group,oxalate group and HCA group.Control group was NRK-52E cells without special treatment;Oxalate group was treated with 600μmol/l oxalate potassium;HCA group was NRK-52E cells treated with 0.5μmol/l HCA for 1 hour,then treated with 600μmol/l oxalate potassium.CCK-8 method was used to detect Cell viability,LDH cytotoxicity assay kit was used to detect cell damage,MDA lipid oxidation assay kit was used to detect cell lipid peroxidation damage,and Western blot was used to detect the expression of antioxidant stress related proteins(SOD 1,SOD2,SOD3 and CAT).Results:1.The effects of and HCA on the viability of NRK-52E cellsCompared with the control group,the cell viability of oxalate group decreased,the difference was statistically significant(P<0.05).With the increase of oxalate concentration and treatment time,cell viability decreased more.Compared with oxalate group,the cell viability of HCA group was significantly higher(P<0.05).2.The effect of oxalate and HCA on the release rate of LHD in NRK-52E cellsThe LDH release rate of oxalate group was higher than that of control group(P<0.05),and the LDH release rate of HCA group was lower than that of oxalate group(P<0.05).3.The effect of oxalate and HCA on MDA content of NRK-52E cellsMDA content in oxalate group was higher than that in control group,the difference was statistically significant(P<0.05),MDA content in HCA group was lower than that in oxalic acid group,the difference was statistically significant(P<0.05).4.The effect of oxalate and HCA on the expression of SOD and CAT in NRK-52E cellsCompared with the control group,oxalate group expressed less SOD1,SOD2 and CAT(P<0.05),and more SOD3(P<0.05).Compared with oxalate group,HCA group expressed more SOD1 and CAT(P<0.05),less SOD3(P<0.05).The difference of SOD2 expression was not statistically significant(P>0.05).Conclusion:Oxalate can reduce the expression of SOD1,SOD2 and CAT,aggravate the oxidative stress of NRK-52E cells,and cause oxidative stress injury.The degree of injury is related to oxalate concentration and treatment time of oxalate.Hydroxycitrate can increase the expression of SOD1 and CAT,enhance the antioxidant capacity of NRK-52E cells,and inhibit the hyperoxalate-induced NRK-52E cells oxidative stress injury.