Journal: Cell Death & Disease

Article Title: Effects of short-chain fatty acids in inhibiting HDAC and activating p38 MAPK are critical for promoting B10 cell generation and function

doi: 10.1038/s41419-021-03880-9

Figure Lengend Snippet: A Purified splenic B cells were polarized to Bregs after a 2-day coculture with indicated SCFAs or Trichostatin A (TSA, an HDAC inhibitor with high efficiency) in the presence of LPS; the nuclear protein was prepared and tested for HDAC inhibition by ELISA. B – D B10 cell frequency in purified splenic B cells cultured with or without sodium acetate ( B ), HDAC inhibitors TSA or vorinostat ( C ), or HAT inhibitor (HATi) anacardic acid ( D ) under the existence of CD40 mAb or LPS for 2 days. Results were shown as representative FACS plots or bar graphs. The data are presented as mean ± SD from three independent experiments. * P < 0.05, ** p < 0.01, and *** p < 0.001 compared to Ctrl or as indicated.

Article Snippet: In some experiments, cells were treated with inhibitors or metabolites, including HDACis TSA (1–10 nM; Beyotime) and vorinostat (100–500 nM; MCE), GPR41 agonist AR420626 (1–10 μM; APExBIO), GPR43 agonist (1–10 μM; Sigma-Aldrich) or antagonist GLPG0974 (500 nM; Sigma-Aldrich), GPR109A agonist niacin (1 mM; Sigma-Aldrich), HAT inhibitor anacardic acid (1–10 μM; MCE), ERK1/2 inhibitor U0126 (5 μM; MCE), p38 inhibitor SB 203580 (5 μM; MCE), or JNK inhibitor SP600125 (1 μM; MCE).

Techniques: Purification, Inhibition, Enzyme-linked Immunosorbent Assay, Cell Culture