Fig 1: Effect of prenatal Poly I:C exposure on the mRNA expression of histone acetyltransferases (HATs) and deacetylases (HDACs). (A) Gcn5, (B) Pcaf, (C) P300, (D) Crebbp, (E) Tip60, (F) Hdac2, (G) Hdac4, and (H) Hdac6. Data were presented as mean ± SEM (n = 6 per group). NS, no significance; *p < 0.05, **p < 0.01; Poly I:C vs. Control.
Fig 2: Potential epigenetic histone acetylation mechanisms for elevated neuroinflammation caused by prenatal Poly I:C exposure in the prefrontal cortex of female juvenile offspring rats. The activation of the NF-?B/NLRP3 inflammatory pathway induced by prenatal Poly I:C exposure may via ? activating histone acetyltransferases (HATs) of EP300 (p300) and CBP (Crebbp), which thus enhances histone H3 and H4 acetylation on the promoter region of Rela, a subunit of NF-?B, ? activating histone deacetylases of HDAC6 (Hdac6), which increases HDAC6-mediated NLRP3 transcriptional activation.
Fig 3: Correlations between the mRNA expression between (A) Nlrp3 and Hdac6, (B) Rela and p300, and (C) Rela and Crebbp.
Fig 4: Enrichment of Hdac6 on the promoter region of Nlrp3. Data were presented as mean ± SEM (n = 6/group). *p < 0.05, Poly I:C vs. Control.
Fig 5: Time-dependent trends of HDAC6 and acetylation α-tubulin protein levels in rats at acute intracerebral hemorrhage.Western blot analysis (A), quantification analysis of HDAC6 (B), and acetylated α-tubulin (C) in an ICH animal model. Values are indicated by means ± SEM; vs. sham, *p < 0.05; **p < 0.01; ***p < 0.001.
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