To investigate the protective effect of astaxanthin (ASTA) on gouty chondrocyte injury induced by monosodium urate crystal (MSU) and its mechanism.

The gout cell model by sodium urate crystals was established. C-28I2 cells were randomly divided into blank group (conventional culture), model group (200 μg·mL^-1 MSU), experimental-L group (200 μg·mL^-1 MSU+20 μmol·mL^-1 ASTA), experimental-H group (200 μg·mL^-1 MSU+40 μmol·L^-1 ASTA), experimental-H+Vector group (transfected with Vector +200 μg·mL^-1 MSU+40 μmol·L^-1 ASTA), experimental-H+NLRP3 group (transfected with NLRP3 plasmid +200 μg·mL^-1 MSU+40 μmol·L^-1 ASTA). Cell counting kit-8 (CCK-8) assay was used to detect the cell proliferation rate; Western blot assay was used to detect the expression of related proteins; the levels of Hyp and GAG were detected by enzyme-linked immunosorbent assay (ELISA).

The cell proliferation rate of blank group, model group, experimental-L group and experimental-H group were (100.00±5.40)%, (67.41±4.52)%, (72.69±5.05)% and (81.47±7.73)%, respectively. The above indicators showed statistically significant differences between the model group and the blank group, between the experimental-L, experimental-H groups and the model group (all P<0.05). Nucleotide binding oligomeric domain-like receptor protein 3 (NLRP3) protein expression levels in blank group, model group, experimental-L group, experimental-H group, experimental-H+Vector group and experimental-H+NLRP3 group were 0.44±0.04, 0.86±0.06, 0.72±0.10, 0.52±0.03, 0.51±0.03 and 1.13±0.10, respectively; the expression levels of cleaved Caspase-1 (Cl-caspase-1) protein were 0.33±0.05, 0.73±0.08, 0.61±0.07, 0.42±0.04, 0.39±0.04 and 0.70±0.06, respectively; the mature interleukin (m-IL)-1β protein expression levels were 0.26±0.03, 0.91±0.05, 0.70±0.11, 0.57±0.08, 0.58±0.06 and 0.79±0.08, respectively; the Hyp levels were (1.95±0.22), (3.33±0.25), (2.53±0.18), (2.22±0.21), (2.24±0.20) and (3.25±0.38) μg·mL^-1, respectively; the GAG levels were (2.30±0.20), (3.71±0.26), (3.29±0.33), (2.90±0.16), (2.97±0.24) and (3.50±0.34) ng·mL^-1, respectively. The above indicators showed statistically significant differences between the model group and the blank group, between the experimental-L, experimental-H groups and the model group, between the experimental-H+NLRP3 group and the experimental-H+Vector group (all P<0.05).

Astaxanthin can regulate NLRP3 to play an anti-inflammatory role and has a protective effect on MSU-induced gouty cartilage injury.