Inhibiting Effect of Lithium Chloride on Endotoxin-induced Uveitis in Rats

Ocul Immunol Inflamm. 2018;26(5):798-806. doi: 10.1080/09273948.2016.1269932. Epub 2017 Jan 12.

Abstract

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.

Keywords: Cytokines; endotoxin-induced uveitis; glycogen synthase kinase 3β; iris-ciliary body; lithium chloride.

MeSH terms

  • Adjuvants, Immunologic / therapeutic use
  • Animals
  • Aqueous Humor / metabolism*
  • Blotting, Western
  • Carrier Proteins / biosynthesis
  • Carrier Proteins / genetics
  • Ciliary Body / metabolism*
  • Ciliary Body / pathology
  • Disease Models, Animal
  • Enzyme-Linked Immunosorbent Assay
  • Gene Expression Regulation / drug effects
  • Intracellular Signaling Peptides and Proteins
  • Iris / metabolism*
  • Iris / pathology
  • Lithium Chloride / therapeutic use*
  • Male
  • Rats
  • Rats, Wistar
  • Real-Time Polymerase Chain Reaction
  • Transcription Factor RelA / biosynthesis
  • Transcription Factor RelA / genetics
  • Tumor Necrosis Factor-alpha / biosynthesis
  • Tumor Necrosis Factor-alpha / genetics
  • Uveitis / chemically induced
  • Uveitis / drug therapy*
  • Uveitis / genetics

Substances

  • Adjuvants, Immunologic
  • Carrier Proteins
  • Intracellular Signaling Peptides and Proteins
  • Transcription Factor RelA
  • Tumor Necrosis Factor-alpha
  • glycogen synthase kinase 3 binding protein, rat
  • Lithium Chloride