Astaxanthin attenuates joint inflammation induced by monosodium urate crystals

Abstract

Gouty arthritis is the one of the most painful arthritis and is caused by an inflammatory reaction. This study investigated whether astaxanthin (AXT), which has documented anti-inflammatory and antioxidant properties, exhibits protective effects against monosodium urate (MSU) crystal-induced inflammation. Cell viability of J774A.1 murine macrophages was assessed by AXT dose-dependent incubation by MTT assays, and expression levels of iNOS and COX-2 proteins as well as secretion of IL-1β were also analyzed under MSU crystals stimulation with or without AXT treatment. The production of inflammatory mediators was found to significantly decrease with AXT treatment, and the formation of the inflammasome complex was also attenuated when cells were co-stimulated with MSU crystals and AXT. Furthermore, we found that expression of the MAPK pathway was downregulated in J774A.1 cells. AXT also inhibited the induction of COX-2 and IL-6 in human chondrocytes and synovial fibroblasts by western blots. Finally, an MSU crystal intra-articular injection rat model for gouty arthritis was utilized in which treatment groups received 5-daily intraperitoneal injections of AXT prior to MSU crystal stimulation, or once intraarticular injections of AXT following MSU crystal stimulation for 6 hours. Results of synovitis score analysis revealed that inflammation was significantly attenuated in the group which received intraperitoneal AXT injection prior to MSU crystal stimulation compared to the group which received MSU only. These results indicate that 11216 |

Astaxanthin Protects Dendritic Cells from Lipopolysaccharide-Induced Immune Dysfunction

“…Astaxanthin provided a neuroprotection against diabetes-induced sickness behavior through inhibiting inflammation [ 30 ]. Astaxanthin also can attenuate monosodium urate crystal-induced arthritis by suppressing the level of pro-inflammatory cytokines [ 31 ]. Moreover, astaxanthin was shown to suppress LPS-induced inflammatory factors increase, MAPK phosphorylation, and NF-kB activation in vivo [ 32 ].…”

Ameliorative Effects of Cardamonin on Monosodium Urate-Induced Gouty Arthritis through Inhibiting NLRP3 Inflammasome Mediation

“…J774A.1 macrophage cells were cultured in Dulbecco’s modified Eagle’s medium (DMEM) high-glucose medium (Gibco, Carlsbad, CA, USA) supplemented with 10% fetal bovine serum (FBS) (Gibco, Carlsbad, CA, USA), 2 mM L-glutamine, 10,000 U/mL penicillin, 10 mg/mL streptomycin, and 25 μg/mL amphotericin at 37 °C in a 5% CO 2 incubator. Cells were subcultured twice weekly using standard protocols [ 30 ].…”

“…Macrophage cells were further treated with 20 μL of 0.5 mg/mL MTT (Sigma-Aldrich, St. Louis, MO, USA) for 3 h, and formazan crystals (Sigma-Aldrich, St. Louis, MO, USA) were then solubilized with 150 μL of dimethyl sulfoxide (DMSO) (Sigma-Aldrich, St. Louis, MO, USA). Absorbance was recorded at 570 nm using the Synergy HT plate reader (Bio-Tek Instruments Inc., Winooski, VT, USA) [ 30 ].…”

“…Membranes were rewashed thoroughly, after which binding was detected using the enhanced chemiluminescence plus western blotting detection system (Merck), in accordance with the manufacturer’s instructions. The membranes were scanned and analyzed via densitometry (VisionWorks LS, UVP, CA, USA), in accordance with the manufacturer’s instructions [ 29 , 30 ].…”

“…Rats in the prevention group underwent intraperitoneal injection of cardamonin (2.5 mg/kg) every day for five days followed by an intra-articular injection of MSU crystals into the knee joint at 24 h prior to sacrifice. Rats in the treatment group underwent an intra-articular injection of MSU (100 μL of 1 mg/mL MSU crystals) and then, 6 h later, underwent an intraperitoneal injection of 50 μL of 10 μM of cardamonin at 18 h prior to sacrifice [ 30 , 31 ].…”