Cynarin suppresses gouty arthritis induced by monosodium urate crystals

Bioengineered

Bo Kong¹  Tao Jiang¹  Xiaobing Xi¹  Hao Tian¹  Wei Yan¹  Changgui Wu¹  Hao Xu²  Shaohua Chen²  Qi Shi²  Yang Liu²  Qianqian Liang²  Yongjun Wang²  Zhaoyi Liu³ 

[1] Department of Orthopaedics, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China;Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China;Shanghai Guanghua Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai, China;

关键词: Cynarin;    gouty arthritis;    JNK;    NF-κB;    NLRP3 inflammasomes;   

DOI  :  10.1080/21655979.2022.2072055

来源: DOAJ

【 摘 要 】

The study is aimed to determine the effects of cynarin (Cyn) on mice with gouty arthritis (GA) induced by monosodium urate (MSU). We measured swelling in the hind paws of mice in vivo using Vernier calipers and ultrasound. The liver, kidney, and hind paws were stained with hematoxylin-eosin, and M1 type macrophages were detected in the hind paws using anti-F4/80 and anti-iNOS antibodies. The mRNA expression of inflammatory factors in bone marrow-derived macrophages (BMDMs) and in the hind paws was detected via quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain containing 3 (NLRP3) inflammasomes and the nuclear factor kappa B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways were analyzed via western blotting. Cyn was detected in vitro using Cell Counting Kit-8 (CCK-8). Cyn treatment reduced hind paw swelling and M1 macrophage infiltration, suppressed the mRNA expression of inflammatory factors, and inhibited NLRP3 inflammasome activation in vivo, in addition to inhibiting the phosphorylation of IKKa/β, p65, and c-Jun NH 2-terminal kinase (JNK). Furthermore, Cyn exerted anti-inflammatory and anti-swelling effects in mice with GA by regulating the NF-κB and JNK pathways and NLRP3 inflammasomes.

【 授权许可】

Unknown