hdac3 inhibitor rgfp966  (TargetMol)

Journal: International Journal of Nanomedicine

Article Title: LincRNA-p21: A Double-Edged Sword in Ethanol-Induced Liver Damage and Its Nanoparticle Solution

doi: 10.2147/IJN.S577455

Figure Lengend Snippet: ALKBH5/lincRNA-p21/FGFR2 promotes autophagy in response to ethanol-induced liver injury. ( A ) HepG2 cells were treated with/without 10 μM SAHA, 10 μM NaB, or 5 μM RGFP966 for 24 h, the expression of lincRNA-p21 was evaluated by RT-PCR. n=3. ( B ) The potential m 6 A sites in lincRNA-p21 predicted using SRAMP. ( C ) m 6 A RNA methylation levels of HepG2 cells with/without alcoholic hepatocyte injury ( P >0.05). n=6. ( D ) When HepG2 cells were exposed to ethanol, the expressions of lincRNA-p21, ALKBH5 and METTL3 were evaluated. The expressions of lincRNA-p21 and ALKBH5 were all down-regulated when HepG2 cells were exposed to 100 mM ethanol ( P <0.01, P <0.05). ( E ) The location of lincRNA-p21 in HepG2 cells demonstrated by the lincRNA-p21 FISH Probe. Scale bars: 50 μm. ( F ) The expressions of lincRNA-p21 was upregulated by ALKBH5 overexpression. n=3. ( G ) LincRNA-p21 was significantly enriched in ALKBH5-bound RNA. n=3. ( H )The methylation level of the 1237 nt site in lincRNA-p21 was evaluated using MeRIP-PCR. n=3. ( I ) Schematic diagram of ALKBH5 mediating m 6 A demethylation and upregulation of lincRNA-p21. The red downward arrow indicates decreased expression. ( J ) The mRNA and protein expression of FGFR2 was evaluated by RT-PCR and Western blot. FGFR2 protein was up-regulated by the overexpression of lincRNA-p21 (FGFR2/β-actin: 0.54 vs 0.20, P =0.001). ( K ) Fluorescence images of the autophagosomes. Scale bars: 10 μm. ( L ) Cell viability was evaluated using a CCK8 assay. n=3. Data represent mean±s.e.m. Significance was determined by two-tailed Student’s t -test. * P <0.05, ** P <0.01, *** P <0.001.

Article Snippet: The HDAC inhibitors Vorinostat (SAHA)(#HY-10221, MCE, USA), sodium butyrate (NaB)(#S1999, Selleck, USA), and HDAC3 inhibitor RGFP966 (#HY-13909, MCE, USA) were used to study the mechanism of lincRNA-p21 regulation.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Methylation, Over Expression, Western Blot, Fluorescence, CCK-8 Assay, Two Tailed Test

Journal: Frontiers in Medicine

Article Title: Investigating the causal relationship of lipid metabolism in polycystic ovary syndrome: a Mendelian randomization study on the regulatory role of 3-Hydroxybutyrate in gene expression

doi: 10.3389/fmed.2026.1747593

Figure Lengend Snippet: (A) 3-HB; (B) RGFP966. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: HDAC3-specific inhibitor RGFP966 (MCE, Catalog No. HY-13909), 3-Hydroxybutyrate (MCE, Catalog No. HY-113378).

Techniques:

Journal: Journal of Advanced Research

Article Title: Kaempferol alleviates myocardial ischemia injury by reducing oxidative stress via the HDAC3-mediated Nrf2 signaling pathway

doi: 10.1016/j.jare.2024.10.037

Figure Lengend Snippet: KAE alleviates myocardial injury and oxidative stress by inhibiting HDAC3. (A and B) The effect of KAE on the mRNA and protein expression of HDAC3 in the myocardial tissue of rats was determined. Data are presented as mean ± SEM (n = 6). ** P < 0.01 vs. vehicle group, # P < 0.05, ## P < 0.01 vs. ISO-treated group. (C and D) The effect of KAE on HDAC3 expression in CoCl 2 -stimulated H9c2 cell. H9c2 cells were pretreated with RGFP966, and then treated with KAE followed by incubation with CoCl 2 for 24 h. (E and F) Cell viability and LDH concentration in culture supernatants were measured. (G and H) The levels MDA and SOD in cell homogenates were determined. (I and J) ROS production was measured using the DCFH-DA. (K and L) The effect of HDAC3 overexpression on ROS production was detected using the DHE. Data are presented as mean ± SEM (n = 3). ** P < 0.01 vs. vehicle group, # P < 0.05, ## P < 0.01 vs. CoCl 2 -treated group, $ P < 0.05, $ $ P < 0.01 vs . KAE and CoCl 2 co-treatment group.

Article Snippet: The HDAC3 specific inhibitor RGFP966 and Nrf2 inhibitor ML385 were from Selleck (Houston, USA).

Techniques: Expressing, Incubation, Concentration Assay, Over Expression

Journal: Journal of Advanced Research

Article Title: Kaempferol alleviates myocardial ischemia injury by reducing oxidative stress via the HDAC3-mediated Nrf2 signaling pathway

doi: 10.1016/j.jare.2024.10.037

Figure Lengend Snippet: KAE alleviates myocardial ischemia injury by reducing oxidative stress via the HDAC3-mediated Nrf2 signaling pathway. (A-C) The Nrf2 expression in myocardial tissue were measured by immunofluorescence and qRT-PCR, respectively. Data are presented as mean ± SEM (n = 6). ** P < 0.01 vs. vehicle group, # P < 0.05, ## P < 0.01 vs. ISO-treated group. (D-F) The effect of KAE on Nrf2 expression in CoCl 2 -stimulated H9c2 cell was determined. (G and H) The effect of Nrf2 inhibition on ROS generation in CoCl 2 -induced H9c2 cells. (I-K) The effect of RGFP966 on Nrf2 expression in KAE-treated H9c2 cells. (L-N) The effect of HDAC3 overexpression on Nrf2 expression in KAE-treated H9c2 cells. (O) Immunoprecipitation of protein from H9c2 cells treated with RGFP966. (P) The effect of HDAC3 overexpression on the acetylation level of Nrf2 in KAE-treated H9c2 cells. Data are presented as mean ± SEM (n = 3). * P < 0.05, ** P < 0.01 vs. vehicle group, # P < 0.05, ## P < 0.01 vs. CoCl 2 -treated group, $ P < 0.05, $ $ P < 0.01 vs. KAE and CoCl 2 co-treatment group.

Article Snippet: The HDAC3 specific inhibitor RGFP966 and Nrf2 inhibitor ML385 were from Selleck (Houston, USA).

Techniques: Expressing, Immunofluorescence, Quantitative RT-PCR, Inhibition, Over Expression, Immunoprecipitation