Huang Danyun, Li Zhijun, Chen Yue, Fan Yan, Yu Tao
Dermatology, The Second Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, 310005, Zhejiang, China.
Department of Internal Medicine, Huangyan District Hospital of Traditional Chinese Medicine, Taizhou, 318020, Zhejiang, China.
Genes Genomics. 2021 Jun;43(6):623-631. doi: 10.1007/s13258-021-01083-2. Epub 2021 Mar 29.
The activation of macrophages and the release of inflammatory cytokines are the main reasons for the progress of systemic lupus erythematosus (SLE). MicroRNA (miRNA)-124 is involved in the regulation of macrophages and is a key regulator of inflammation and immunity.
To explore whether paeoniflorin (PF) regulates the biological functions of macrophages depends on miR-124.
RT-PCR, WB, ELISA, CCK-8 and flow cytometry were used to evaluate that PF regulated the biological functions of THP-1 cells through miR-124.
PF significantly inhibited the proliferation while promotes the apoptosis of THP-1 cells, and inhibited the release of IL-6, TNF-α and IL-1βin THP-1 cells. RT-PCR results shown that PF up-regulated the expression of miR-124 in THP-1 cells. Functional recovery experiments showed that compared with the LPS + mimic-NC group, LPS + miR-124 mimic significantly inhibited the proliferation and the release of IL-6, TNF-α and IL-1β, but promoted the apoptosis of THP-1 cells. In addition, compared with the LPS + PF + inhibitor-NC group, LPS + PF + miR-124 inhibitor significantly promoted the proliferation and the release of IL-6, TNF-α and IL-1β, but inhibited the apoptosis of THP-1 cells.
By down-regulating miR-124, PF inhibits the proliferation and inflammation of THP-1 cells, and promotes the apoptosis of THP-1 cells.
巨噬细胞的激活和炎性细胞因子的释放是系统性红斑狼疮(SLE)病情进展的主要原因。微小RNA(miRNA)-124参与巨噬细胞的调节,是炎症和免疫的关键调节因子。
探讨芍药苷(PF)对巨噬细胞生物学功能的调节是否依赖于miR-124。
采用RT-PCR、WB、ELISA、CCK-8和流式细胞术评估PF通过miR-124调节THP-1细胞的生物学功能。
PF显著抑制THP-1细胞增殖,促进其凋亡,并抑制THP-1细胞中IL-6、TNF-α和IL-1β的释放。RT-PCR结果显示,PF上调THP-1细胞中miR-124的表达。功能恢复实验表明,与LPS+模拟物-NC组相比,LPS+miR-124模拟物显著抑制THP-1细胞增殖及IL-6、TNF-α和IL-1β的释放,但促进THP-1细胞凋亡。此外,与LPS+PF+抑制剂-NC组相比,LPS+PF+miR-124抑制剂显著促进THP-1细胞增殖及IL-6、TNF-α和IL-1β的释放,但抑制THP-1细胞凋亡。
PF通过下调miR-124抑制THP-1细胞增殖和炎症反应,并促进THP-1细胞凋亡。