Immunohistochemical localization for nuclear factor kappa B p50 in cochlea of mice
- VernacularTitle:小鼠耳蜗核因子-κB p50免疫组化定位
- Author:
Sun JIANHE
;
Yang WEIYAN
;
Sha SHUHUA
;
Jochen SCHACHT
- Publication Type:Journal Article
- Keywords:
transcription factors;
NF-κB p50;
cochlea;
immunohistochemisty;
lipopolisaccharides
- From:Medical Journal of Chinese People's Liberation Army
2007;32(1):1-4
- CountryChina
- Language:Chinese
-
Abstract:
Objective To show the capability of NF-κB expression in cochlea. Methods Kanamycin (KA) was subcutaneously injected twice daily for 3 and 7 days with an eight hours interval between two injections, and lipopolysaccharide (LPS) was injected into the tympanic cavity of mice. Equal amount of saline was injected for 7 days as control. Frozen sections of all mice cochleae were examined immmunohistochemichally with rabbit polyclonal NF-κB p50. Expression of NF-κB p50 immunoreactivity of mouse cochleae is identified as showed as brown reaction products characteristic of DAB immunohistochemistry. Results Immnoreactivity NF-κB p50 in mouse cochlea was localized in the organ of Corti, spiral limbus, tectorial membrane, the vascular stria, spiral ligament, spiral ganglion and nerve fibers. The immunoreaction could be observed in all spirals throughout the cochlea. Stronger staining was visible in spiral ligament, tectorial membrane, spiral prominence, spiral ganglion and nerve fibers, and the organ of Corti. The immunoreaction in the vascular stria was weaker than that in the structures mentioned above. The immunoreaction in the organ of Corti was observed in inner hair cells (IHC) and outer hair cells (OHC), inner and outer pillar cells, Deiter's cells, and Boettcher's cells. The immunoreaction was weaker in inner sulcus cells, Hensen's cells and Claudius'cells. The stronger immunoreaction was observed in nucleus of spiral ganglion cells. The nucleus of IHC and OHC remained unstained. Conclusion The injection of LPS/KA can promote NF-κB p50 expression to induce an acute reaction in mouse cochlea.
