The protective effect of sinapic acid in osteoarthritis: In vitro and in vivo studies

被引:30
作者
Li, Xiaobin [1 ,2 ]
Lin, Jian [1 ,2 ]
Ding, Xiaoxia [3 ]
Xuan, Jiangwei [1 ,2 ]
Hu, Zhichao [1 ,2 ]
Wu, Dengying [1 ,2 ]
Zhu, Xingyu [4 ]
Feng, Zhenhua [5 ]
Ni, Wenfei [1 ,2 ]
Wu, Aimin [1 ,2 ]
机构
[1] Wenzhou Med Univ, Dept Orthopaed Surg, Affiliated Hosp 2, Wenzhou, Peoples R China
[2] Wenzhou Med Univ, Yuying Childrens Hosp, Wenzhou, Peoples R China
[3] Wenzhou Med Univ, Affiliated Hosp 1, Dept Chemoradiat Oncol, Wenzhou, Peoples R China
[4] Wenzhou Med Univ, Clin Med Sch 2, Wenzhou, Peoples R China
[5] Jiaxing Univ, Dept Orthopaed Surg, Affiliated Hosp 2, Jiaxing, Peoples R China
基金
中国国家自然科学基金;
关键词
chondrocytes; IL-1; beta; inflammation; NF-kappa B; Nrf2; sinapic acid; NF-KAPPA-B; SIGNALING PATHWAY; KNEE; DEGRADATION; CHONDROCYTES; PROGRESSION; ACTIVATION; EXPRESSION; ADAMTS-4; NRF2;
D O I
10.1111/jcmm.14096
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The anti-inflammatory effect of sinapic acid (SA) has been reported in several studies. However, whether SA has the same effect on osteoarthritis (OA) has yet to be clearly elucidated. We designed a series of in vitro and in vivo procedures to verify the above conjecture. Compared with controls, SA-pretreated human chondrocytes showed lower levels of interleukin (IL)-1 beta-induced IL-6, prostaglandin E2 (PGE2), nitric oxide (NO) and tumour necrosis factor-alpha (TNF-alpha) in vitro. Meanwhile, SA could also reverse the degradation of type II collage and aggrecan, as well as the overproduction of matrix metalloproteinase-9 (MMP-9) and matrix metalloproteinase-13 (MMP-13), inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2 and a disintegrin and metalloproteinase thrombospondin motifs (ADAMTS)-5. Furthermore, activation of nuclear factor kappa B (NF-kappa B), which was induced by IL-1 beta, was also inhibited by SA through the pathway of nuclear factor-erythroid 2-related factor-2 (Nrf2)/heme oxygenase 1. In vivo, SA could delay the progress of mice OA models. We propose that SA may be applied as a potential therapeutic drug in OA treatment.
引用
收藏
页码:1940 / 1950
页数:11
相关论文
共 35 条
  • [1] Altman RD, 2000, ARTHRITIS RHEUM-US, V43, P1905
  • [2] COX-2, NO, and cartilage damage and repair.
    Amin A.R.
    Dave M.
    Attur M.
    Abramson S.B.
    [J]. Current Rheumatology Reports, 2000, 2 (6) : 447 - 453
  • [3] Antioxidant effects of phenolic rye (Secale cereale L.) extracts, monomeric hydroxycinnamates, and ferulic acid dehydrodimers on human low-density lipoproteins
    Andreasen, MF
    Landbo, AK
    Christensen, LP
    Hansen, Å
    Meyer, AS
    [J]. JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY, 2001, 49 (08) : 4090 - 4096
  • [4] Sinapic acid modulates Nrf2/HO-1 signaling pathway in cisplatin-induced nephrotoxicity in rats
    Ansari, Mushtaq Ahmad
    [J]. BIOMEDICINE & PHARMACOTHERAPY, 2017, 93 : 646 - 653
  • [5] Osteoarthritis, angiogenesis and inflammation
    Bonnet, CS
    Walsh, DA
    [J]. RHEUMATOLOGY, 2005, 44 (01) : 7 - 16
  • [6] Redox activation of Nrf2 & NF-κB: A double end sword?
    Buelna-Chontal, Mabel
    Zazueta, Cecilia
    [J]. CELLULAR SIGNALLING, 2013, 25 (12) : 2548 - 2557
  • [7] Histone deacetylase inhibition activates Nrf2 and protects against osteoarthritis
    Cai, Dawei
    Yin, Shasha
    Yang, Jun
    Jiang, Qing
    Cao, Wangsen
    [J]. ARTHRITIS RESEARCH & THERAPY, 2015, 17
  • [8] Sinapic Acid and Its Derivatives as Medicine in Oxidative Stress-Induced Diseases and Aging
    Chen, Chunye
    [J]. OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2016, 2016
  • [9] Anti-arthritic effects of chlorogenic acid in interleukin-1β-induced rabbit chondrocytes and a rabbit osteoarthritis model
    Chen, Wei-Ping
    Tang, Jing-Li
    Bao, Jia-Peng
    Hu, Peng-Fei
    Shi, Zhong-Li
    Wu, Li-Dong
    [J]. INTERNATIONAL IMMUNOPHARMACOLOGY, 2011, 11 (01) : 23 - 28
  • [10] Cooper C, 2000, ARTHRITIS RHEUM, V43, P995, DOI 10.1002/1529-0131(200005)43:5<995::AID-ANR6>3.0.CO