ABSTRACT

We investigated if Red ginseng extract (RGE) suppressed monosodium urate crystal (MSU)-induced NLRP3 activation and could be a potential therapeutic agent for gout. The effects of RGE on acute gouty inflammation were investigated using the air-pouch model. RGE significantly suppressed acute gout inflammation in the air-pouch model, based on the decreased number of WBCs in the air-pouch lavage fluid. In vitro, RGE inhibited MSU-induced IL-1β production in THP-1 cells. Twenty-four gout patients in intercritical period were randomized either to red ginseng tablet (RGT) or placebo group. The assembly of NLRP3 inflammasomes was inhibited via reduced ASC expression and oligomerization. Patients taking RGT for 3 months showed significantly reduced NLRP3 expression compared to baseline. In conclusion, RGE suppressed acute gout inflammation by suppressing NLRP3 inflammasomes in animal models. Clinically, RGT suppressed NLRP3 expression in gout patients. The data suggest that red ginseng may exert an additive benefit in gout treatment.

摘要

我们调查了红参提取物（RGE）是否抑制了尿酸钠（MSU）诱导的NLRP3活化，并且可能是痛风的潜在治疗剂。使用气袋模型研究了RGE对急性痛风炎症的影响。基于气囊灌洗液中白细胞数量的减少，RGE在气囊模型中显着抑制了急性痛风炎症。在体外，RGE抑制MSU诱导的THP-1细胞中IL-1β的产生。危重期的24名痛风患者被随机分为红参片（RGT）或安慰剂组。NLRP3炎性小体的组装可通过减少ASC表达和寡聚来抑制。与基线相比，服用RGT 3个月的患者显示NLRP3表达明显降低。结论，RGE通过抑制动物模型中的NLRP3炎性小体来抑制急性痛风炎症。临床上，RGT抑制痛风患者的NLRP3表达。数据表明，红参可以在痛风治疗中发挥附加作用。