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FLEXA是一种新型草药配方,通过抑制MAPK/NF-κB信号通路的激活来减轻骨关节炎的炎症和软骨降解。

FLEXA, a new herbal formulation, alleviates inflammation and cartilage degradation of osteoarthritis by inhibiting the activation of the MAPK/ NF-κB signaling pathways.

作者信息

Song Minwoo, Choi You Yeon, Jin Seong Chul, Baek Hee Kyung, Yi Seungyob, Kim Eun Jung, Yang Woong Mo

机构信息

Department of Convergence Korean Medical Science, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

KHU-KIST Department of Converging Science and Technology, College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

出版信息

Fitoterapia. 2025 May 11;184:106590. doi: 10.1016/j.fitote.2025.106590.

Abstract

BACKGROUND

Osteoarthritis (OA) is a progressive musculoskeletal disorder marked by cartilage degradation and inflammation. FLEXA, a novel herbal formulation composed of Ostericum koreanum Maxim, Cibotium barometz J. Smith, and Carthamus tinctorius Linne, has traditionally been used to manage joint-related conditions. This study aimed to evaluate the therapeutic efficacy of FLEXA in an OA model by elucidating its molecular mechanisms and multi-target effects.

METHODS

Network pharmacology analysis was performed to identify potential interactions between the active components of FLEXA and OA-related targets. Osteoarthritis was induced in rats via intra-articular injection of monosodium iodoacetate (MIA), followed by intramuscular administration of FLEXA at two doses (0.0094 and 0.094 mg/kg) twice weekly for four weeks. Cartilage integrity, proteoglycan content, bone mineral density, and inflammatory markers were assessed. Additionally, the effects of FLEXA on mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) pathways were evaluated in interleukin-1β-stimulated SW1353 chondrocytes.

RESULTS

FLEXA improved cartilage integrity, increased proteoglycan levels, and enhanced bone mineral density in the femoral condyles of OA rats. Network pharmacology revealed that FLEXA modulated key targets associated with "Positive Regulation of Extracellular Matrix Assembly". In SW1353 cells, FLEXA suppressed MAPK and NF-κB signaling, reducing pro-inflammatory cytokine production and extracellular matrix degradation.

CONCLUSION

These findings demonstrate that FLEXA exerts multi-target chondroprotective and anti-inflammatory effects, suggesting its potential as a complementary therapeutic option for OA management.

摘要

背景

骨关节炎(OA)是一种以软骨降解和炎症为特征的进行性肌肉骨骼疾病。FLEXA是一种由朝鲜独活、金毛狗脊和红花组成的新型草药配方,传统上用于治疗关节相关疾病。本研究旨在通过阐明其分子机制和多靶点作用来评估FLEXA在OA模型中的治疗效果。

方法

进行网络药理学分析,以确定FLEXA的活性成分与OA相关靶点之间的潜在相互作用。通过关节内注射碘乙酸钠(MIA)诱导大鼠骨关节炎,随后每周两次肌肉注射两种剂量(0.0094和0.094mg/kg)的FLEXA,持续四周。评估软骨完整性、蛋白聚糖含量、骨矿物质密度和炎症标志物。此外,在白细胞介素-1β刺激的SW1353软骨细胞中评估FLEXA对丝裂原活化蛋白激酶(MAPK)和核因子-κB(NF-κB)信号通路的影响。

结果

FLEXA改善了OA大鼠股骨髁的软骨完整性,提高了蛋白聚糖水平,并增强了骨矿物质密度。网络药理学显示,FLEXA调节与“细胞外基质组装的正向调节”相关的关键靶点。在SW1353细胞中,FLEXA抑制MAPK和NF-κB信号传导,减少促炎细胞因子的产生和细胞外基质的降解。

结论

这些发现表明,FLEXA具有多靶点软骨保护和抗炎作用,提示其作为OA管理的辅助治疗选择的潜力。

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