NACHT, LRR and PYD domains-containing protein 3 inflammasome is activated and inhibited by berberine via toll-like receptor 4/myeloid differentiation primary response gene 88/nuclear factor-κB pathway, in phorbol 12-myristate 13-acetate-induced macrophages

作者：Huang, Zhouqing^*; Ye, Bozhi; Han, Jibo; Kong, Fanqi; Shan, Peiren; Lu, Zhongqiu; Huang, Weijian^*

来源：Molecular Medicine Reports, 2018, 17(2): 2673-2680.

DOI：10.3892/mmr.2017.8189

• berberine
• NACHT
• LRR and PYD domains-containing protein 3
• inflammasome
• monocytes
• macrophages
• nuclear factor-kappa B signaling pathway
• atherosclerosis

The nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP-3) inflammasome has recently emerged as a pivotal regulator of chronic inflammation. The present study investigated the expression of NLRP3 inflammasome in phorbol 12-myristate 13-acetate (PMA)-induced macrophages, and aimed to identify the effects of berberine on the inflammasome. Human monocytic THP-1 cells were pretreated with berberine for 1 h and then induced with PMA for 48 h. Total RNA and protein were collected for reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Supernatants were collected to determine IL-beta 1 levels by using ELISA. The present study demonstrated that NLRP3 inflammasome and IL-1 beta were activated in PMA-induced macrophages in a time-dependent manner, whereas berberine significantly inhibited their expression in a dose-dependent manner in PMA-induced macrophages. Furthermore, berberine also suppressed the toll-like receptor 4 (TLR4)/myeloid differentiation primary response gene 88 (Myd88)/nuclear factor (NF)-kappa B signaling pathway which was activated during the conversion of THP-1 cells to macrophages by PMA. In conclusion, berberine reduced NLRP3 inflammasone expression by suppressing the activation of the TLR4/Myd88/NF-kappa B signaling pathway in PMA-induced macrophages. This inhibitory effect may imply an important role of berberine on chronic inflammation and atherogenic progression in coronary artery disease.

• 出版日期2018-2
• 单位温州医科大学