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hdac3 inhibitor rgfp966  (MedChemExpress)


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    Structured Review

    MedChemExpress hdac3 inhibitor rgfp966
    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 <t>RGFP966</t> 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.
    Hdac3 Inhibitor Rgfp966, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hdac3+inhibitor+rgfp966/RGFP966/pmc12915450-38-13-17
    Average 95 stars, based on 69 article reviews
    hdac3 inhibitor rgfp966 - by Bioz Stars, 2026-09
    95/100 stars

    Images

    1) Product Images from "LincRNA-p21: A Double-Edged Sword in Ethanol-Induced Liver Damage and Its Nanoparticle Solution"

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

    Journal: International Journal of Nanomedicine

    doi: 10.2147/IJN.S577455

    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.
    Figure Legend 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.

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

    Related Articles

    Mouse Assay:

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity.
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraper itoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraperitoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Sterility:

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity.
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraper itoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraperitoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Injection:

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity.
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraper itoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Article Title: HDAC3 Mediates Hippocampal Microglial Pyroptosis Via the STING/NLRP3 Pathway and Contributes To Cognitive Impairment in Sepsis-Associated Encephalopathy
    Article Snippet: .. The HDAC3 inhibitor RGFP966 (20 mg/kg, HY-13909, MedChemExpress, Monmouth Junction, NJ, USA) or vehicle was administered to mice via subcutaneous injection. ..

    Article Title: Desaminotyrosine promotes tuft cell expansion and integrates intestinal type 2 immunity
    Article Snippet: .. Mice were assigned to three groups: (i) normal group mice received sterile water as drinking water for 7 days; (ii) DAT group mice were administered the 200 mM DAT solution as drinking water for 7 days; (iii) DAT + RGFP966 group mice were intraperitoneally injected with the Hdac3 inhibitor RGFP966 (HY-13909, Med Chem Express) 15 mg/kg one day before the start of DAT treatment. ..

    Histone Deacetylase Assay:

    Article Title: LincRNA-p21: A Double-Edged Sword in Ethanol-Induced Liver Damage and Its Nanoparticle Solution
    Article Snippet: .. Histone Deacetylase (HDAC) Inhibitor Treatment 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. ..



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    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 <t>RGFP966</t> 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.
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    KAE alleviates myocardial injury and oxidative stress by inhibiting <t>HDAC3.</t> (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 <t>RGFP966,</t> 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.
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    Image Search Results


    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.

    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

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

    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:

    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.

    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

    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.

    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