Kallikrein-binding protein promotes axonal regeneration and protect rat retinal ganglion cells following optic nerve injury.
- Author:
Shun-xiang JIN
1
;
Yong ZENG
;
Jing WAN
;
Kun WAN
;
Yuan-yuan LI
;
Li-yan LI
;
Ting-hua WANG
;
Zhong-tang FENG
;
Yan LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Axons; physiology; Female; GAP-43 Protein; metabolism; Nerve Regeneration; drug effects; physiology; Neuroprotective Agents; pharmacology; Optic Nerve Injuries; drug therapy; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells; drug effects; physiology; Serpins; pharmacology
- From: Journal of Southern Medical University 2010;30(4):738-741
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of kallikrein-binding protein (KPB) in protecting retinal ganglion cells (RGCs) and promoting axonal regeneration following optical nerve injury in rats.
METHODSCrush injury of the optic nerve at 0.5-1.0 mm from the eyeball was induced in rats, which received subsequent KBP injection into the vitreous cavity (experimental group) and PBS injection (control group). At 7, 14 and 21 days after the injury, the rats were sacrificed and frozen sections of the eyeball were prepared to observe the structure and thickness of the retina and count the number of survival RGCs with HE staining. The optic nerves were collected for Western blotting to assess the effect of KBP on the RGCs and axonal regeneration.
RESULTSRGC counts and retinal thickness showed significant differences between the two groups. Western blotting also demonstrated a significant difference in the expression of the nerve regeneration marker protein GAP-43 between the two groups.
CONCLUSIONKBP offers protection on RGCs and promotes regeneration of the optic nerve axons after optic nerve injury in rats.
