Current eye research · 2013
The neuroprotective effect of carnosine (β-alanyl-L-histidine) on retinal ganglion cell following ischemia-reperfusion injury.
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Ji Yong-Sok, Park Jung-Won, Heo Hwan, Park Jong-Seong, Park Sang-Woo
Аннотация
PURPOSE: To investigate whether carnosine can increase retinal ganglion cell (RGC) survival in ischemic mouse retina.
METHODS: Retinal ischemia was induced by constant elevation of intraocular pressure (100-110 mmHg) for 60 min in C57BL/6 J mice pretreated with carnosine (1000 mg/kg) or saline. Hypoxia inducing factor-1 alpha (HIF-1α), glial fibrillary acidic protein (GFAP), and dynamin-related protein-1 (Drp-1) expressions were assessed at 6, 12, and 24 h after retinal ischemia. Bax and Bcl-2 expressions were also analyzed at 12 h after retinal ischemia. RGC survival was assessed by retrograde FluoroGold labeling at 2 weeks after retinal ischemia.
RESULTS: The expression of HIF-1α, GFAP, and Drp-1 was increased within 24 h after ischemic injury. Carnosine treatment effectively decreased the elevated expression of HIF-1α, GFAP, and Drp-1 in ischemic mouse retina. In ischemic retina treated with carnosine, Bax expression was decreased, whereas Bcl-2 expression was increased compared with ischemic retina treated with saline. Carnosine treatment also protected against RGC loss in ischemia mouse retina.
CONCLUSIONS: Our findings showed that carnosine treatment significantly decreased RGC loss through decreased expression of HIF-1α, GFAP, Drp-1, and Bax, and increased expression of Bcl-2 in ischemic mouse retina. We suggest that carnosine can be an effective endogenous neuroprotective molecule in the prevention of RGC loss in ischemic retina.
METHODS: Retinal ischemia was induced by constant elevation of intraocular pressure (100-110 mmHg) for 60 min in C57BL/6 J mice pretreated with carnosine (1000 mg/kg) or saline. Hypoxia inducing factor-1 alpha (HIF-1α), glial fibrillary acidic protein (GFAP), and dynamin-related protein-1 (Drp-1) expressions were assessed at 6, 12, and 24 h after retinal ischemia. Bax and Bcl-2 expressions were also analyzed at 12 h after retinal ischemia. RGC survival was assessed by retrograde FluoroGold labeling at 2 weeks after retinal ischemia.
RESULTS: The expression of HIF-1α, GFAP, and Drp-1 was increased within 24 h after ischemic injury. Carnosine treatment effectively decreased the elevated expression of HIF-1α, GFAP, and Drp-1 in ischemic mouse retina. In ischemic retina treated with carnosine, Bax expression was decreased, whereas Bcl-2 expression was increased compared with ischemic retina treated with saline. Carnosine treatment also protected against RGC loss in ischemia mouse retina.
CONCLUSIONS: Our findings showed that carnosine treatment significantly decreased RGC loss through decreased expression of HIF-1α, GFAP, Drp-1, and Bax, and increased expression of Bcl-2 in ischemic mouse retina. We suggest that carnosine can be an effective endogenous neuroprotective molecule in the prevention of RGC loss in ischemic retina.
Предметные рубрики MeSH
AnimalsBiomarkersBlotting, WesternCarnosineCell CountCell SurvivalDynaminsFluorescent Antibody Technique, IndirectGlial Fibrillary Acidic ProteinHypoxia-Inducible Factor 1, alpha SubunitInjections, IntraperitonealMiceMice, Inbred C57BLNerve Tissue ProteinsNeuroprotective AgentsProto-Oncogene Proteins c-bcl-2Reperfusion InjuryRetinal DiseasesRetinal Ganglion Cellsbcl-2-Associated X Protein