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TNF-alpha-induced optic nerve degeneration and nuclear factor-kappaB p65.
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OBJECTIVE
To characterize a model of optic nerve axonal degeneration induced by tumor necrosis factor (TNF)-alpha and to determine the role of nuclear factor (NF)-kappaB p65 in axonal degeneration.
METHODS
Groups of rats were euthanatized at 1 day, 1 or 2 weeks, or 1 or 2 months after intravitreal
Calbindin-D28K expression induced by glial cell line-derived neurotrophic factor in substantia nigra neurons dependent on PI3K/Akt/NF-kappaB signaling pathway.
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Calbindin-D28K is a calcium-binding protein in neuronal cytoplasm, which has the capability to protect neurons from degeneration. It was reported that glial cell line-derived neurotrophic factor (GDNF) increased calbindin-D28K expression in dopaminergic neurons in vitro. It was observed in our
The effect of 17beta-estradiol on IL-6 secretion and NF-kappaB DNA-binding activity in human retinal pigment epithelial cells.
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Toll-like receptors (TLRs) and inflammatory cascades participate in the pathology of age-related macular degeneration (AMD). The effect of estrogens on the development of AMD is poorly understood, although many studies indicate that these compounds can modulate inflammatory responses. In this study,
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