Analysis of the Relevance between t-BHP Induced Apoptosis and STATs mRNA Expression in HEI-OC1 Cells / 听力学及言语疾病杂志
Journal of Audiology and Speech Pathology
; (6): 162-166, 2018.
Article
in Chinese
| WPRIM (Western Pacific)
| ID: wpr-698123
Responsible library:
WPRO
ABSTRACT
Objective To study the biological effects of (Janus Kinase-Signal transducers and activators of transcription,AK-STATs)path-way in hair cell apoptosis by analyzing the expression level of signal transducers and activators of transcription (STATS) of apoptotic HEI-OC1 cells line induced by oxidative stress injury.Methods Using different poisoning concentrations (0,20,40,60μM) of(Tert-Butyl hydroperoxide,T-BHP) built the apoptotic HEI-OC1 cells model while 0 μM was used as the control group.The apoptosis level at different poisoning concentration groups was detected by Annexin V-FITC/PI and the expression level of STATs mRNA by real-time quantitative PCR detecting system.Results The apoptosis rates in different contamination groups(0,20,40,60 μM) were 3.9%,7.4%,32.0%,and 91.2%,respectively.Compared with control group,STAT1 mRNA,STAT3 mRNA,STATS mRNA,and STAT6 mRNA expression levels in different poisoning concentration groups declined significantly (F=5 534.302,P<0.01;F=146.038,P<0.01;F=685.929,P<0.01;F=516.11,P< 0.01).No statistically significant differences were found among the poisoning concentration groups (P>0.05).Compared with the control group,the STAT2 mRNA expression levels changed significantly (F=1 259.148,P< 0.01).The STAT2 mRNA expression level in 20 μM contamination group decreased while 40,60 μM contamination group increased significantly (P<0.01).No expression of STAT4 in HEI-OC1 cell was noted.Conclusion The JAK-STAT2 signal pathway has the biological effects on leading oxidative stress injury apoptosis and JAK-STAT1/STAT3/STAT5/STAT6 has the biological effect of inhibit oxidative stress injury apoptosis.
Full text:
Available
Database:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Journal of Audiology and Speech Pathology
Year:
2018
Document type:
Article