Valproic acid attenuates inflammation of optic nerve and apoptosis of retinal ganglion cells in a rat model of optic neuritis.

摘要: Abstract Aims Optic neuritis (ON) is an inflammatory disease of the optic nerve, which often occurs in patients with multiple sclerosis (MS) and leads to retinal ganglion cell (RGC) death even severe visual loss. Valproic acid (VPA) a short-chain branched fatty anti-epileptic, neuro-protective anti-inflammatory effects. Here, we examined effects VPA experimental autoimmune encephalomyelitis (EAE) rats explored underlying mechanisms. Main methods EAE was induced by subcutaneous injection myelin basic protein, emulsified complete Freund’s adjuvant Mycobacterium tuberculosis H37Ra into Lewis rats. Subsequently, animals groups were treated orally (250 or 500 mg/kg) once day for 13 days. Key findings treatment significantly attenuated inflammation microgliosis nerve EAE-ON rats, as evidenced decrease mRNA levels interferon (INF)-γ, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-17, inducible nitric oxide synthase (iNOS), suppression nuclear (NF)-κB signal pathway well down-regulation CD11b expression nerve. Additionally, apoptotic RGCs remarkably increased retina, inhibited treatment. Consistent TUNEL staining, administration also obviously suppressed ratio Bax: Bcl-2 cleaved caspase-3 PARP Significance Our demonstrated that could prevent responses RGC apoptosis suggesting may be available protection during ON.