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首页|期刊导航|山东医药|活血化瘀中药调控VEGF信号通路抑制血管翳生成治疗类风湿关节炎的研究进展

活血化瘀中药调控VEGF信号通路抑制血管翳生成治疗类风湿关节炎的研究进展

刘婷 赵啸虎 刘源 姜萍 考希良

山东医药2026,Vol.66Issue(3):154-158,5.
山东医药2026,Vol.66Issue(3):154-158,5.DOI:10.3969/j.issn.1002-266X.2026.03.032

活血化瘀中药调控VEGF信号通路抑制血管翳生成治疗类风湿关节炎的研究进展

Research progress on traditional Chinese medicines for promoting blood circulation and removing blood stasis regulating VEGF signaling pathway to inhibit pannus formation in rheumatoid arthritis

刘婷 1赵啸虎 1刘源 1姜萍 1考希良1

作者信息

  • 1. 山东中医药大学第一临床医学院,山东济南 250014
  • 折叠

摘要

Abstract

Rheumatoid arthritis(RA)is a common chronic autoimmune disease,with main pathological features in-cluding synovial inflammation and hyperplasia,antibody production,invasive neovascular pannus formation,and destruc-tive changes in cartilage and bone.Pannus,a key link in RA pathology,is regulated by vascular endothelial growth factor(VEGF).Traditional Chinese medicines for promoting blood circulation and removing blood stasis[Danshen(Salvia milti-orrhiza),Zicao(Lithospermum erythrorhizon),and Chuanshanlong(Dioscorea nipponica),etc.],and their compound formulas including Qingre Huoxue Formula,Yuxuebi Tablet,Ersi Decoction,etc.can improve the"blood stasis"state,regulate the VEGF pathway,inhibit pannus formation,and delay RA progression.A deeper understanding of their mecha-nisms and clinical value in inhibiting pannus via regulating the VEGF pathway provides theoretical support for the integra-tive treatment of RA with traditional Chinese and Western medicine.

关键词

活血化瘀类中药/血管翳/血管内皮生长因子/类风湿关节炎

Key words

traditional Chinese medicines for promoting blood circulation and removing blood stasis/pannus/vascu-lar endothelial growth factor/rheumatoid arthritis

分类

医药卫生

引用本文复制引用

刘婷,赵啸虎,刘源,姜萍,考希良..活血化瘀中药调控VEGF信号通路抑制血管翳生成治疗类风湿关节炎的研究进展[J].山东医药,2026,66(3):154-158,5.

基金项目

国家自然科学基金面上项目(82274481) (82274481)

国家中医药管理局科技司共建科技项目(GZY-KJS-SD-2023-041) (GZY-KJS-SD-2023-041)

山东省卫生健康科创团队建设项目(2024sdskctd-03) (2024sdskctd-03)

山东省自然科学基金(ZR2022LZY004) (ZR2022LZY004)

齐鲁医派中医学术流派传承项目[鲁卫函(2022)93号]. (2022)

山东医药

1002-266X

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