Journal
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
Volume 118, Issue -, Pages 357-364Publisher
ELSEVIER
DOI: 10.1016/j.ijbiomac.2018.06.032
Keywords
Cerebral ischemia; L-homocarnosine; Inflammation; Antioxidants; Rats
Funding
- Hainan Natural Science Foundation [818QN247, 818MS066]
- Hainan Province Key RD Project [ZDYF2018154]
- National Natural Science Foundation of China [81460550]
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We investigated the therapeutic effects of L-homocarnosine against inflammation in a rat model of cerebral ischemia-reperfusion injury. Rats were grouped into control, middle cerebral artery occlusion (MCAO), 0.5 mM L-homocarnosine + MCAO, and 1 mM L-homocarnosine + MCAO treatment groups. Superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase, lipid peroxidation, and reduced glutathione (GSH) levels were measured. Neurological scores were assessed, and histopathology, scanning electron microscopy (SEM), and fluorescence microscopy analyses were conducted. The mRNA expression levels of nod-like receptor protein 3 (NLRP3), tumor necrosis factor alpha (TNF-alpha), and interleukin-6 (IL-6) and protein expression levels of NLRP3 were assessed. L-Homocarnosine supplementation substantially increased SOD, catalase, Gpx, and GSH levels, whereas it reduced the levels of lipid peroxidation relative to MCAO rats. L-Homocarnosine significantly reduced the infarct area and neurological deficit score, as well as histopathological alteration, apoptosis, and necrosis in brain tissue. The mRNA expression levels of NLRP3, TNF-alpha, and IL-6 were increased in MCAO rats, whereas L-homocarnosine supplementation reduced mRNA expression by >40%, and NLRP3 protein expression was reduced by >30% in 1 mM L-homocarnosine-treated MCAO rats. We propose that L-homocarnosine exerts a protective effect in cerebral ischemia-reperfusion injury-induced rats by downregulating NLRP3 expression. (C) 2018 Elsevier B.V. All rights reserved.
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