Figure 1.

Neuroprotection against hypoxic stress via 1400W.

(A) Schematic overview of cobalt chloride induced hypoxia and the effects on the eye. Cobalt chloride induces hypoxia via hypoxia-inducible factor alpha (Hif-1α), resulting in increased inducible nitric oxide synthase (iNOS) expression, and nitric oxide (NO) production. NO causes an increase in the mRNA expression of HSP70 and iNOS and regulates HIF-1α. This results in a loss of retinal neurons. (B) Overview of the retinal layers and the effects of cobalt chloride and treatment with the iNOS-inhibitor 1400W. Cobalt chloride increased apoptosis and loss of microglia, retinal ganglion, amacrine, and bipolar cells. Basically, all neurons of the inner retina and the microglia were affected. The iNOS-inhibitor prevented apoptosis and loss of retinal ganglion and bipolar cells, but not damage to microglia and amacrine cells. RGC: Retinal ganglion cells; ROS: reactive oxygen species.