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. 2021 Dec 29;12(5):2280–2299. doi: 10.1016/j.apsb.2021.12.014

Figure 4.

Figure 4

Cur inhibits the P300–BRD4 pathway by attenuating ROS generation through TFEB-activated autophagy. (A) ChIP analysis of the enrichment of P300, BRD2, BRD3, BRD4 and H3 at −1 kb from the promoter, at the promoter and at +1 kb from the promoter regions of inflammatory genes (IL-8, IL-1β, TNF-α) in Cur-treated FCs combined with siTFEB. (B) Immunoblot analysis of the expressions of P300, BRD2, BRD3, BRD4, Actin, acetyl-H3, and H3 in Cur-treated FCs combined with siTFEB. (C, D) Immunoblot of acetyl-H3, H3, BRD4 and actin in FCs treated with siATG5 and Cur (C) or the reactive oxygen species (ROS) scavenger NAC (D). (E) The ROS level in FCs treated with Cur in the presence of siTFEB or siATG5 was detected using the DCFH-DA probe. Scale bar = 50 μm. Data are expressed as mean ± SEM, n = 5. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001; #P < 0.05, ##P < 0.01, ###P < 0.001.