http://www.jcps.ac.cn

Journal of Chinese Pharmaceutical Sciences ›› 2019, Vol. 28 ›› Issue (2): 100-113.DOI: 10.5246/jcps.2019.02.010

• Original articles • Previous Articles     Next Articles

Curcumin inhibits inflammatory cytokine transcription via the apoptosis pathway in THP-1 cells

Jianwei Gao, Feng Ye*   

  1. Department of Pharmacology, Beijing Anzhen Hospital, Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing 100029, China
  • Received:2018-11-10 Revised:2018-12-15 Online:2019-02-28 Published:2019-01-02
  • Contact: Tel.: +86-010-64456560, E-mail: yf0441@126.com
  • Supported by:

    National Natural Science Foundation of China (Grant No. 81202543).

Abstract:

To investigate the anti-inflammatory mechanism of curcumin in THP-1 cells induced by LPS, the effect of curcumin on inflammatory cytokine mRNA expression was assessed by Real-time PCR. Covalent post-translational modification profiles were determined by a PathScan® Kit. Western blotting analysis verified the PathScan results and the effects of curcumin on nucleus-relatedprotein changes. Annexin V-FITC and PI staining was used to detect early cellular apoptosis by flow cytometry. Anti-inflammatory effects of curcumin were mediated by reducing the levels of IL-1β, IL-6, TNF-α and ICAM-1 mRNA. However, PathScan and Western blotting results showed that curcumin inhibited inflammatory cytokine mRNA expressions by preventing p65 nuclear translocation without interfering with p38 and JNK/MAPK phosphorylation or IκBα degradation. Moreover, curcumin promoted PARP-1 cleavage and inhibited intranuclear lamina protein Lamin B1 expression. Flow cytometry results showed that curcumin enhanced Annexin V-FITC positive cells when LPS induced inflammation. This study provided evidence that curcumin inhibited p65 nuclear translocation and cytokine transcription by regulating nuclear protein structure and function, suggesting that early apoptosis involved the suppression of p65 nuclear translocation. 

Key words: Curcumin, Inflammation, Cytokine, NF-κB, Apoptosis

CLC Number: 

Supporting: