Sunflower Receptacle Extract Alleviates Acute Gouty Arthritis via HMGB1-TLR4-NLRP3 Inflammatory Pathway
- 1College of Chinese Medicinal Materials, Jilin Agricultural University, Changchun 130118, China
- 2Institute of Special Animal and Plant Sciences, Chinese Academy of Agricultural Sciences, Changchun 130112, China
- 3Dong-E Ejiao Health Industry Technology Co., Ltd., Liaocheng 252201, China
Abstract
Background/Objectives: Acute gouty arthritis (AGA) is an auto-inflammatory disorder characterized by dysregulated innate immune activation and overactive NOD-like receptor family pyrin domain-containing 3 (NLRP3)/Toll-like receptor 4 (TLR4) inflammatory signaling. While adverse effects limit current therapies, the mechanism by which sunflower receptacle extract (SPE) alleviates gout remains unclear. Methods: This study investigated the anti-inflammatory mechanism of SPE in a male SPF-grade SD rat model of AGA induced by intra-articular monosodium urate crystals. Rats were orally administered SPE or colchicine, and ankle joint swelling, synovial histopathology, serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β), and interleukin-6 (IL-6), and synovial protein expression were assessed. Western blotting was used to assess the expression of the high-mobility group box 1 (HMGB-1), TLR4, and mitogen-activated protein kinase (MAPK) signaling pathways, as well as the activation of NLRP3. Results: Compared to the AGA group, treatment with colchicine and SPE significantly reduced ankle joint swelling, improved inflammatory infiltration in synovial tissue, and lowered serum levels of inflammatory factors TNF-α, IL-1β, and IL-6 (p < 0.05, p < 0.01). They also markedly decreased the expression of HMGB-1 and proteins in the TLR4, nuclear factor-ĸB (NF-ĸB), and MAPK pathways in joint synovial tissue (p < 0.05, p < 0.01, p < 0.001). Conclusions: SPE markedly reduced joint swelling and synovial inflammatory infiltration, lowered serum TNF-α, IL-1β, and IL-6 levels, and decreased synovial expression of HMGB-1, TLR4, MyD88, TRAF6, and NF-ĸB. Moreover, SPE suppressed NLRP3 inflammasome assembly and MAPK pathway activation. These results indicate that SPE mitigates AGA by inhibiting the HMGB-1-TLR4-NLRP3 inflammatory axis.
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BibTeX
@article{li2026sunflower,
title = {{Sunflower Receptacle Extract Alleviates Acute Gouty Arthritis via HMGB1-TLR4-NLRP3 Inflammatory Pathway}},
author = {Zhiman Li and Zhilong Li and Xiaohui Huo and Xinyuan Wang and Yinshi Sun},
journal = {Nutrients},
year = {2026},
month = oct,
doi = {10.3390/nu18193290},
url = {https://europepmc.org/article/PMC/PMC13667103},
note = {CC BY},
}
RIS
TY - JOUR
TI - Sunflower Receptacle Extract Alleviates Acute Gouty Arthritis via HMGB1-TLR4-NLRP3 Inflammatory Pathway
AU - Zhiman Li
AU - Zhilong Li
AU - Xiaohui Huo
AU - Xinyuan Wang
AU - Yinshi Sun
PY - 2026
DA - 2026/10/01
JO - Nutrients
DO - 10.3390/nu18193290
UR - https://europepmc.org/article/PMC/PMC13667103
AB - Background/Objectives: Acute gouty arthritis (AGA) is an auto-inflammatory disorder characterized by dysregulated innate immune activation and overactive NOD-like receptor family pyrin domain-containing 3 (NLRP3)/Toll-like receptor 4 (TLR4) inflammatory signaling. While adverse effects limit current therapies, the mechanism by which sunflower receptacle extract (SPE) alleviates gout remains unclear. Methods: This study investigated the anti-inflammatory mechanism of SPE in a male SPF-grade SD rat model of AGA induced by intra-articular monosodium urate crystals. Rats were orally administered SPE or colchicine, and ankle joint swelling, synovial histopathology, serum levels of tumor necrosis factor-α (TNF-α), interleukin-1β(IL-1β), and interleukin-6 (IL-6), and synovial protein expression were assessed. Western blotting was used to assess the expression of the high-mobility group box 1 (HMGB-1), TLR4, and mitogen-activated protein kinase (MAPK) signaling pathways, as well as the activation of NLRP3. Results: Compared to the AGA group, treatment with colchicine and SPE significantly reduced ankle joint swelling, improved inflammatory infiltration in synovial tissue, and lowered serum levels of inflammatory factors TNF-α, IL-1β, and IL-6 (p < 0.05, p < 0.01). They also markedly decreased the expression of HMGB-1 and proteins in the TLR4, nuclear factor-ĸB (NF-ĸB), and MAPK pathways in joint synovial tissue (p < 0.05, p < 0.01, p < 0.001). Conclusions: SPE markedly reduced joint swelling and synovial inflammatory infiltration, lowered serum TNF-α, IL-1β, and IL-6 levels, and decreased synovial expression of HMGB-1, TLR4, MyD88, TRAF6, and NF-ĸB. Moreover, SPE suppressed NLRP3 inflammasome assembly and MAPK pathway activation. These results indicate that SPE mitigates AGA by inhibiting the HMGB-1-TLR4-NLRP3 inflammatory axis.
SN - 2072-6643
ER -