It has been demonstrated that peripheral infections accompanied by neuroinflammation may modify brain development or affect normal brain aging and represent major risk factors for the development of neurological disorders. A wide range of synthetic and natural compounds with anti-inflammatory properties have been evaluated in animal models of neuroinflammation and neurodegeneration as an adjuvant therapeutic strategy. In the present study we have demonstrated for the first time that sodium thiosulphate (STS), a known antidote approved for treatment of certain medical conditions, is capable of reducing brain inflammation caused by systemic LPS administration. STS reduced brain levels of pro-inflammatory cytokine interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), ionized calcium binding adaptor molecule 1 (Iba-1) and 18 kDa translocator protein (TSPO) in an animal model of systemic LPS-induced neuroinflammation. In addition, we demonstrated for the first time elevated TSPO expression in retinal ganglion cells layer after peripheral LPS challenge and inhibition of ocular TSPO expression after treatment with STS. We think that STS may be used as an adjuvant anti-inflammatory therapy for many pathological conditions associated with inflammation in the brain.
Keywords: Cyclooxygenase-2; Interleukin-1β; Lipopolysaccharide; Neuroinflammation; Peripheral infection; Sodium thiosulphate.