Objective To investigate the role of mitochondrial calcium uniporter(MCU)in oxidative stress injury in HEI-OC1 cells.Methods H2O2 was used to establish the HEI-OC1 oxidative stress damage model,which were divided into the normal control group,H2 O2 group and H2 O2+Ru360(MCU inhibitor)group.The cell viabil-ity of each group was detected by CCK-8 reagent.State of oxidative stress was detected by flow cytometry.Mito-chondrial membrane potential(MMP)and mitochondrial Ca2+levels were observed by applying JC-1 probe and Rhod-2/AM probe,respectively.The protein expression levels of MCU,Drp1,MFN1 and MFN2 were detected by Western blot.Results HEI-OC1 cells of H2 O2 group showed a significant decrease in cell viability with oxidative stress injury.Cellular ROS accumulation,MMP loss accompanied by mitochondrial calcium overload,elevated MCU protein expression,Drp1 mitochondrial translocation and reduced MFN1 and MFN2 expression.In the cells of H2O2+Ru360 group,the high expression of MCU was inhibited,cell viability was increased and ROS levels were reduced.Besides,the mitochondrial Ca2+levels were reduced and mitochondrial homeostasis was restored.Com-pared with the H2O2 group,the differences were all statistically significant(P＜0.05).Conclusion MCU is in-volved in oxidative stress injury in HEI-OC1 cells,and inhibition of MCU may alleviate cellular stress by improving mitochondrial dynamics-related homeostasis.

Objective To investigate the role of mitochondrial calcium uniporter(MCU)in oxidative stress injury in HEI-OC1 cells.Methods H2O2 was used to establish the HEI-OC1 oxidative stress damage model,which were divided into the normal control group,H2 O2 group and H2 O2+Ru360(MCU inhibitor)group.The cell viabil-ity of each group was detected by CCK-8 reagent.State of oxidative stress was detected by flow cytometry.Mito-chondrial membrane potential(MMP)and mitochondrial Ca2+levels were observed by applying JC-1 probe and Rhod-2/AM probe,respectively.The protein expression levels of MCU,Drp1,MFN1 and MFN2 were detected by Western blot.Results HEI-OC1 cells of H2 O2 group showed a significant decrease in cell viability with oxidative stress injury.Cellular ROS accumulation,MMP loss accompanied by mitochondrial calcium overload,elevated MCU protein expression,Drp1 mitochondrial translocation and reduced MFN1 and MFN2 expression.In the cells of H2O2+Ru360 group,the high expression of MCU was inhibited,cell viability was increased and ROS levels were reduced.Besides,the mitochondrial Ca2+levels were reduced and mitochondrial homeostasis was restored.Com-pared with the H2O2 group,the differences were all statistically significant(P＜0.05).Conclusion MCU is in-volved in oxidative stress injury in HEI-OC1 cells,and inhibition of MCU may alleviate cellular stress by improving mitochondrial dynamics-related homeostasis.

Objective To investigate the distribution of blaOXA-51-like genes and the clonal relation-ship among Acinetobacter baumannii strains isolated from three teaching hospitals in Guangzhou , China. Methods Fifty-two Acinetobacter baumannii isolates were genotyped by multilocus sequence typing (MLST).eBURST algorithm was performed to define clonal complexes (CCs).blaOXA-51-like genes were am-plified by using polymerase chain reaction ( PCR) and sequenced .Results MLST grouped the A.bauman-nii isolates into 5 existing sequence types (STs) and 7 new STs.STn4 carried allele G1 with a T→C muta-tion at the 3rd nucleotide site (nt3) on the gpi111 locus.STn5 carried allele A1, possessing A→C muta-tions at nt156 and nt159 on the gltA1 locus.ST195 and ST208 accounted for 69.2%of all isolates.Clonal relationship analysis showed that ST 195 and ST208 belonged to CC92.Fifty-one A.baumannii isolates car-ried OXA-66 and the rest one carried OXA-199.Conclusion A.baumannii strains that belonged to CC92 and carried OXA-66 were the predominant genotype circulating in Guangzhou , China.