The Role of PP1 in the Cochlea of Mimetic Aging Mice Induced by D -galactose
10.3969/j.issn.1006-7299.2017.02.013
- VernacularTitle:蛋白磷酸酶1在D-半乳糖诱导老化小鼠耳蜗中的表达
- Author:
Tao XU
;
Tingting MA
;
Xidi WU
;
Shuangyue LIU
- Keywords:
Protein phosphatase 1;
D-galactose;
Cochlea;
Age-related hearing loss
- From:
Journal of Audiology and Speech Pathology
2017;25(2):176-179
- CountryChina
- Language:Chinese
-
Abstract:
Objective This study was designed to investigate the expression and potential role of the protein phosphatase 1 (PP1) impairment in D -galactose-induced inner ear aging mouse model .Methods Forty Kunming mice were randomly divided into two groups :the control group and D -galactose group ,20 mice for each .The D-galactose group mice were treated with a daily subcutaneous injection of the D -galactose solutions (800 mg · kg -1 · d-1 ) or an equal volume of normal saline(for the control group) in the nape back for 8 weeks .Eight weeks after D-galactose administration ,the effects of were measured by total Superoxide Dismutase (SOD) activity and Malon-dialdehyde (MDA) level in plasma .Immunofluoresence was performed to detect the location of the PP1 expression in the cochlea .Real-time PCR was performed to detect the level of PP1 mRNA in cochlea .A Western blot analysis was performed to analyze the protein levels of protein phosphates 1 nuclear targeting subunit (PNUTS) ,PP1 and caspase-3 in the inner ear .Results The MDA level was more significantly increased in the D -galactose group than in the control group ;however ,the total SOD activity was significantly decreased in the plasma of D -galactose- induced aging mice(P<0 .01) .The results showed that PP1 was predominantly localized in the nucleus and cyto-plasm of the hair cell ,spiral ganglion cell and stria vascularis cell .And the protein levels of PP1 and caspase-3 sig-nificantly increased ,and the level of PNUTS was decreased in the cochlea of the D -galactose group when compared to the control group .Conclusion PP1 contributes to the development of D -galactose-induced aging mice .
