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Inhibiting Effect of Lithium Chloride on Endotoxin-induced Uveitis in Rats.
PURPOSE: To evaluate the anti-inflammatory effect of lithium chloride in endotoxin-induced uveitis.
METHODS: A total of 200 Wistar rats were randomly divided into four groups: a control group; EIU group; LiCl-treated control group; and LiCl-treated lipopolysaccharide group. Clinical score, slit-lamp photography, hematoxylin and eosin (H&E) staining were used to determine the degree of inflammatory reaction. Level of glycogen synthase kinase3-beta and nuclear factor-kappa B p65 in iris-ciliary body was examined by western blot and RT-PCR. Cytokines in aqueous humor were detected by ELISA.
RESULTS: Pretreatment with LiCl produced an anti-inflammatory effect during endotoxin-induced uveitis (EIU). With LiCl treatment, the level of P-GSK3-β in iris-ciliary body was upregulated and the expression of NF-κB p65 was significantly suppressed during EIU.
CONCLUSIONS: LiCl pretreatment can suppress intraocular inflammatory responses in EIU rats. Mechanistically, this anti-inflammatory effect may be related to the inhibitory phosphorylation of GSK3-β.
METHODS: A total of 200 Wistar rats were randomly divided into four groups: a control group; EIU group; LiCl-treated control group; and LiCl-treated lipopolysaccharide group. Clinical score, slit-lamp photography, hematoxylin and eosin (H&E) staining were used to determine the degree of inflammatory reaction. Level of glycogen synthase kinase3-beta and nuclear factor-kappa B p65 in iris-ciliary body was examined by western blot and RT-PCR. Cytokines in aqueous humor were detected by ELISA.
RESULTS: Pretreatment with LiCl produced an anti-inflammatory effect during endotoxin-induced uveitis (EIU). With LiCl treatment, the level of P-GSK3-β in iris-ciliary body was upregulated and the expression of NF-κB p65 was significantly suppressed during EIU.
CONCLUSIONS: LiCl pretreatment can suppress intraocular inflammatory responses in EIU rats. Mechanistically, this anti-inflammatory effect may be related to the inhibitory phosphorylation of GSK3-β.
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