Morin, a dietary bioflavonol suppresses monosodium urate crystal-induced inflammation in an animal model of acute gouty arthritis with reference to NLRP3 inflammasome, hypo-xanthine phospho-ribosyl transferase, and inflammatory mediators.
The anti-inflammatory effect of morin, a dietary bioflavanol was explored on monosodium urate (MSU) crystal-induced inflammation in rats, an experimental model for acute gouty arthritis. Morin treatment (30mg/kg b.wt) significantly attenuated the ankle swelling and the levels of lipid peroxidation, nitric oxide, serum pro-inflammatory cytokines (tumor necrosis factor (TNF) -α, interleukin (IL)-1β, and IL-6), monocyte chemoattractant protein (MCP)-1, vascular endothelial growth factor (VEGF), prostaglandin E2 (PGE2), and articular elastase along with an increased anti-oxidant status (catalase (CAT) and superoxide dismutase (SOD)) in the joint homogenate of MSU crystal-induced rats. Histological assessment revealed that morin limited the diffusion of joint space, synovial hyperplasia, and inflammatory cell infiltrations. The mRNA expression of NLRP3 (nucleotide oligomerization domain (NOD)-like receptor family, pyrin domain containing 3) inflammasome, caspase-1, pro-inflammatory cytokines, MCP-1, inflammatory enzymes (inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2)), and nuclear factor-kappa B (NF-κB) p65 was found downregulated and HPRT (hypo-xanthine phospho-ribosyl transferase) mRNA expression was upregulated in morin treated MSU crystal-induced rats. In addition, morin treatment reduced the protein expression of NF-κB p65, p-NF-κB p65, iNOS, COX-2, and TNF-α. The results clearly demonstrated that morin exert a potent anti-inflammatory effect on MSU crystal-induced inflammation in rats.
Immunopathology Lab, School of Biosciences and Technology, VIT University, Vellore 632014, Tamil Nadu, India.
Chitra
C
Dhanasekar
Immunopathology Lab, School of Biosciences and Technology, VIT University, Vellore 632014, Tamil Nadu, India. Electronic address: mkr474@gmail.com.
Mahaboobkhan
M
Rasool
D000208:Acute Disease; D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D015210:Arthritis, Gouty / Q000139:chemically induced / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D004032:Diet; D004195:Disease Models, Animal; D005260:Female; D005419:Flavonoids / Q000494:pharmacology* / Q000627:therapeutic use; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D007041:Hypoxanthine Phosphoribosyltransferase / Q000378:metabolism*; D058847:Inflammasomes / Q000378:metabolism*; D018836:Inflammation Mediators / Q000378:metabolism*; D008297:Male; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D010196:Pancreatic Elastase / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013583:Synovial Membrane / Q000187:drug effects / Q000276:immunology; D051996:Transcription Factor RelA / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014527:Uric Acid / Q000009:adverse effects* / Q000737:chemistry; D047309:Flavones
D000975:Antioxidants; D051546:Cyclooxygenase 2; D016207:Cytokines; D005419:Flavonoids; D007041:Hypoxanthine Phosphoribosyltransferase; D058847:Inflammasomes; D018836:Inflammation Mediators; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D052247:Nitric Oxide Synthase Type II; D010196:Pancreatic Elastase; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D014527:Uric Acid; C008548:morin; D047309:Flavones
Acute gouty arthritis; Inflammatory enzymes; NLRP3 inflammasome; Pro-inflammatory cytokine