Effects of acute oxidative stress induced by H2O2 on expression of SMP30 and morphology, survival rate of human lens epithelial cells
10.13389/j.cnki.rao.2017.0078
- VernacularTitle:过氧化氢诱导的急性氧化应激对人晶状体上皮细胞形态、生存率及衰老标记蛋白30(SMP30)表达的影响
- Author:
Shuning LI
;
Xi CHEN
;
Hongkan ZHANG
;
Linzhi JIANG
;
Hao LIANG
;
Shaojian TAN
- Keywords:
senescence marker protein30;
human lens epithelial cells;
acute oxidative stress;
cataract
- From:
Recent Advances in Ophthalmology
2017;37(4):310-313
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of acute oxidative stress induced by H2O2 on expression of senescence marker protein30 (SMP30) and morphology,survival rate of human lens epithelial cells (HLECs).Methods HLECs were treated with H2O2(0 μmol · L-1,100 μmol · L-1,200 μmol · L-1,300 μmol · L-1) for 24 hours,the acute oxidative stress models were established,the changes of cell morphology was observed,and MTT was used to analyze the cells state,the expressions of SMP30 were measured by Western blot.Results The cell density decreased,morphological changed and viability of cells significant decreased in 100 μmol · L-1 and 200 μmol ·L-1 treated group,the large and round cells appeared,the cell body stretched with unclear boundary.With the H2O2 concentration increased,the viability of cells were gradually decreased in treated group,there were statistical differences compared with 0 μmol · L-1 treated group (all P < 0.05).The relative expression of SMP30 in control group and 100 μmol · L-1 and 200 μmol · L-1 treated group were 0.273 ±0.055,0.464 ± 0.058,0.442 ± 0.050,respectively.There were significant differences between 100 μmol · L-1,200 μmol · L-1 treated group and control group (all P < 0.05),and there was no statistical difference between 100 μmol · L-1 and 200 μmol · L-1 treated group (P > 0.05).Conclusion SMP30 is up-regulated in HLECs under acute oxidative stress induced by H2O2,the cell morphology is changed,the viability of cells is decreased,and SMP30 may be involved in the process of acute oxidative stress in HLECs.