ab10583 Acetyl-NF-kappaB p65 (Lys310) Antibody

Western blot analysis of extracts from LPS treated HepG2 cells, using Acetyl-NF-kappaB p65 (Lys310) Antibody. The lane on the left was treated with blocking peptide.

Figure 6.|ABL does not act directly on proinflammatory signaling. (A) p-Akt, p-ERK, p-JNK,p-p38, p-NF-κB and Ac-NF-κB in brain tissues of pAd-miR-155-infected mice and miR-155–/–mice treated with or without ABL (20 mg/kg) were detected by Western blotting, andband intensities that were normalized to β-actin are represented by bar graphs as themeans ± SD (n = 6 per group); *P< 0.05 versus pAd + MCAO; #P< 0.05 versus WT + MCAO.(B) BV2 cells were treated with or without ABL (100 μmol/L) for 24 h prior to OGD. p-Akt, p-ERK, p-JNK, p-p38 and Ac-NF-κB were detected by Western blotting, and band intensities that were normalized to β-actin are represented by bar graphs as the means ± SDfrom three independent experiments; *P< 0.05 versus con group.

Figure 3: | Regulation of MAN on NAMPT and Sirt1 in RAW 264.7 cells in vitro. (a) Expression of iNAMPT in cells; (b) levels of eNAMPT in culture medium; (c) expression of Sirt1 in cells; (d) deacetylation capability of Sirt1 indicated by expression of ace-p65 in cells. Statistical signifcance: ∗p < 0.05 and ∗∗p < 0.01 compared with LPS treated cells.

Figure 3. |Effects of anesthesia and surgery on the levels of DNMT1 and hippocampal neuroinflammation. A. Representative immunoblot bands of DNMT1, ac-NF-κB and IL-6 expression in the hippocampus in CON and ISO+SUR groups.

Fig. 2. Repeated sevoflurane exposure led to downregulation of SIRT1 and the upregulation of acetylated NF-κB in the hippocampi of developing mice. (A) Representative western blots of SIRT1, AC-NF-κB, total NF-κB, GAPDH, nuclear NF-κB and Lamin B proteins. (B–D) Densitometry quantification of SIRT1, AC-NF-κB/NF-κBand nuclear NF-κB. Data are shown as the means ± SEM (n = 5 per group). ∗P < .05, ∗∗P < .01.

Figure 6. |SIRT1 inhibited the decomposition of extracellular matrix in BMP2-induced-C3H10T1/2 cells under oxidative stress. (E, F) The expression of Ac-p65 and p65 among Ad-BMP2, Ad-BMP2+H2O2, and Ad-BMP2+Ad-SIRT1+H2O2 groups. The data are denoted as the mean ± SD. *: p < 0.05, Ad-BMP2+H2O2 vs. Ad-BMP2; #: p < 0.05, Ad-BMP2+Ad-SIRT1+H2O2 vs. Ad-BMP2+H2O2.

FIGURE 2 | Effects of the RvE1 and LXA4 combination on NF-κB modification.(F) Phosphorylation and acetylation levels of p65 and expressions of SIRT1, SIRT6 and SIRT7 protein (normalized to that of β-tubulin) detected by western blotting.

Figure 4 Effect of MG activated CAP-SIRT1 pathway on NF-κB-mediated inflammatory response in rat macrophages. (A) Expression of α7nAChR, SIRT1, ac-p65, p-p65 and p65 in macrophages investigated by immunoblotting; (B–E) quantitative result of (A). #P<0.05, ##P<0.01, ###P<0.001 compared with normal, *P<0.05, **P<0.01, ***P<0.001 compared with AIA rats, &P<0.05 compared with MG (early).

Fig. 2 Effects of empa on NF-kB and SOD2 expression and activation. A Western blot analysis for acetylated, phosphorylated and total form of NF-kB, and acetylated and total form SOD2 in AC16 cells exposed to NG concentration (4.5 mM) (NG), cells exposed to high glucose concentration (HG), and cells co-treated with HG and 0.5 nM of EMPA (HG + Empa). Densitometry analysis was performed using ImageJ 1.52n software. The histograms show the densitometric analysis of 3 separate experiments representing the relative expression being NG value set as 1. Data are mean ± SEM.

Figure 5 MiR-34a-5p aggravated HUVEC inflammation through the NF-κB signaling pathway. (A, B) The protein bands and levels of P65 and Ac-P65 were determined by WB. *P