Lack of Galectin-3 attenuates neuroinflammation and protects the retina and optic nerve of diabetic mice.

摘要: Abstract Diabetic retinopathy is the leading cause of acquired blindness in working-age individuals. Recent work has revealed that neurodegeneration occurs earlier than vascular insult and distal optic nerve damage precedes retinal degeneration insult. Since we have shown reduced after crush Galectin-3 knockout (Gal-3 −/−) mice, decided to investigate whether Gal-3 −/− could relieve inflammation preserve both neurons structure retina following 8 weeks diabetes. Diabetes was induced 2-month-old male C57/bl6 WT or mice by a single injection streptozotocin (160 mg/kg). Histomorphometric analyses showed no gross difference, except for number ganglion cells diabetic correlated increased apoptosis. In nerve, neuroinflammation, suggested smaller Iba1+ cells, particularly amoeboid profiles end. Furthermore, iNOS staining nerves as well GFAP segment nerve. Finally, histomorphometric myelinated fibers higher myelin more rectilinear compared mice. Therefore, present study provided evidence central target stimulates neuroinflammation impairs neurological outcomes visual complications Our findings provide support clinical use inhibitors against near future.