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pka inhibitor h89  (MedChemExpress)


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    MedChemExpress pka inhibitor h89
    PKA inhibition by <t>H89</t> abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .
    Pka Inhibitor H89, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 226 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+h89/H-89/pmc13487505-47-58-64
    Average 97 stars, based on 226 article reviews
    pka inhibitor h89 - by Bioz Stars, 2026-09
    97/100 stars

    Images

    1) Product Images from "NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling"

    Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling

    Journal: Frontiers in Pharmacology

    doi: 10.3389/fphar.2026.1895800

    PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .
    Figure Legend Snippet: PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .

    Techniques Used: Inhibition, Enzyme-linked Immunosorbent Assay, Staining, Fluorescence, Activation Assay, Immunofluorescence

    NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .
    Figure Legend Snippet: NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .

    Techniques Used: Metabolomic, Saline, Control

    Related Articles

    Control:

    Article Title: Effect and mechanism of maternal prolactin levels on depressive-like behavior in prenatally stressed offspring.
    Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

    Injection:

    Article Title: Effect and mechanism of maternal prolactin levels on depressive-like behavior in prenatally stressed offspring.
    Article Snippet: This is a PDF of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability.. This version will undergo additional copyediting, typesetting and review before it is published in its final form.. As such, this version is no longer the Accepted Manuscript, but it is not yet the definitive Version of Record; we are providing this early version to give early visibility of the article.

    Saline:

    Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling
    Article Snippet: .. Treatment regimens were as follows: vehicle-treated mice received equivalent volumes of saline; the LPS group received lipopolysaccharide (LPS; 1 mg/kg; L2880, Sigma-Aldrich, United States); the LPS + NDP-MSH group received LPS (1 mg/kg) together with NDP-MSH (2 mg/kg; HY-N2466, MedChemExpress, United States); the LPS + NDP-MSH + H89 group received LPS (1 mg/kg), NDP-MSH (2 mg/kg), and the PKA inhibitor H89 (10 mg/kg; HY-15979A, MedChemExpress, United States); and the H89-alone group received H89 (10 mg/kg). .. LPS (L2880, Sigma-Aldrich, United States) was dissolved in double-distilled water to prepare a stock solution (5 μg/μL) and stored at 4 °C.

    Cell Culture:

    Article Title: Myeloid Cell-Derived Thrombospondin-1 Mediates Anti-Metastatic Effects of Histamine Dihydrochloride in B16 Melanoma
    Article Snippet: .. In some experiments, primary human monocytes cultured in complete IMDM were treated with 100 μM HDC, 100 μM NMH, 20 μM forskolin (Sigma-Aldrich), 10 nM cholera toxin (Sigma-Aldrich), or 500 μM 8-bromoadenosine 3′,5′-cyclic monophosphate sodium salt (8-bromo-cAMP; Sigma-Aldrich), either alone or in combination with 10 μM of the PKA inhibitor H89 (Medchemexpress). ..

    Article Title: FOSL2-driven SASP in endometrial stroma promotes the inflammation of endometriosis
    Article Snippet: THP-1 cells were cultured in RPMI 1640 medium (Gibco, USA) containing 10% FBS at 37°C in a humidified atmosphere containing 5% CO 2 . .. For signaling pathway investigation, normal euESCs were treated with PGE2 (20 μM, MCE, USA) for 24 h. To assess the role of the cAMP/PKA pathway, EMs-euESCs were cultured for 24 h in the presence of either the adenylyl cyclase inhibitor SQ22536 (100 μM, MCE, USA) or the PKA inhibitor H89 (5 μM, MCE, USA). ..



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    97
    MedChemExpress prka pka inhibitor h89
    PKA inhibition by <t>H89</t> abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .
    Prka Pka Inhibitor H89, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Cell Signaling Technology Inc pka inhibitor h89
    PKA inhibition by <t>H89</t> abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .
    Pka Inhibitor H89, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    MedChemExpress camp pka pathway inhibitor h89
    Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor <t>H89</t> (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.
    Camp Pka Pathway Inhibitor H89, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .

    Journal: Frontiers in Pharmacology

    Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling

    doi: 10.3389/fphar.2026.1895800

    Figure Lengend Snippet: PKA inhibition by H89 abolishes the neuroprotective and antidepressant effects of NDP-MSH. (A) Experimental timeline and grouping strategy. Mice were assigned to Vehicle, LPS, LPS + NDP-MSH(NDP), LPS + NDP-MSH + H89(LNH), or H89 groups. (B) Representative locomotor traces in the OFT. (C) Behavioral assessments. NDP-MSH significantly increased sucrose preference in LPS-treated mice, whereas H89 co-treatment abolished this effect in the SPT. (One-way ANOVA, F (4, 41) = 13.96, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 6.649, p < 0.001; Vehicle vs. LNH: q (41) = 6.804, p < 0.001; LPS vs. NDP: q (41) = 4.128, p < 0.05; NDP vs. LNH: q (41) = 4.237, p < 0.05). NDP-MSH restored total distance traveled reduced by LPS; H89 partly reversed this improvement in the OFT (One-way ANOVA, F (4, 41) = 29.92, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS: q (41) = 13.07, p < 0.0001; Vehicle vs. NDP: q (41) = 7.823, p < 0.0001; Vehicle vs. LNH: q (41) = 11.660, p < 0.0001; LPS vs. NDP, q (41) = 5.225, p < 0.01). NDP-MSH partly restored central zone entries reduced by LPS; H89 partly reversed this improvement in the OFT (Kruskal-Wallis non-parametric test, H (4) = 30.23, p < 0.0001, followed by Dunn's multiple comparisons test. Vehicle vs. LPS: Z = 4.745, p < 0.0001; Vehicle vs. NDP: Z = 2.600, p = 0.093; Vehicle vs. LNH: Z = 3.924, p < 0.0001; H89 vs. LPS: Z = 3.615, p < 0.01) (Veh, n = 8; H89, n = 8; LPS, n = 10; NDP, n = 9; LNH, n = 11). (D) ELISA quantification of IL-1β levels in the PFC. NDP-MSH reversed LPS-induced IL-1β elevation, whereas H89 prevented this effect (One-way ANOVA, F (4, 25) = 18.02, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (25) = 9.990, p < 0.0001; Vehicle vs. LNH: q (25) = 6.190, p < 0.01; LPS vs. NDP, q (25) = 8.350, p < 0.0001; NDP vs. LNH, q (25) = 4.549, p < 0.05) (n = 6 mice per group). (E) Representative images of mPFC neuronal dendrites by Golgi-Cox staining. Scale bar = 20 μm. Column graphs illustrate the relative spine numbers. NDP-MSH significantly increased spine density reduced by LPS treatment, whereas co-treatment with the PKA inhibitor H89 abolished this restorative effect (One-way ANOVA, F (4, 20) = 36.61, p < 0.0001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (20) = 13.07, p < 0.0001; Veh vs. NDP, q (20) = 6.820, p < 0.001; Veh vs. LNH, q (20) = 12.82, p < 0.0001; LPS vs. NDP, q (20) = 6.245, p < 0.01; NDP vs. LNH, q (20) = 5.995, p < 0.01) (n = 5 mice per group, with 4-6 sections per mouse; at least 10 dendritic segments were randomly selected and quantified per section). (F) Quantification of relative Iba-1 fluorescence intensity, NDP-MSH normalized LPS-evoked microglial activation; H89 co-treatment restored microglial density to LPS-like levels (One-way ANOVA, F (4, 10) = 19.57, p < 0.001, followed by Tukey’s multiple comparisons test. Veh vs. LPS, q (10) = 8.650, p < 0.001; Veh vs. LNH, q (10) = 8.412, p < 0.01; LPS vs. NDP, q (10) = 5.940, p < 0.05; NDP vs. LNH, q (10) = 5.702, p < 0.05) (n = 3 mice per group). (G) Representative immunofluorescence images of Iba-1 staining in the mPFC, Scale bar = 100 µm. Data are presented as mean ± SEM. *p < 0.05, **p < 0.01, ***p < 0.001. ****p < 0.0001. Source: BioRender.com .

    Article Snippet: Treatment regimens were as follows: vehicle-treated mice received equivalent volumes of saline; the LPS group received lipopolysaccharide (LPS; 1 mg/kg; L2880, Sigma-Aldrich, United States); the LPS + NDP-MSH group received LPS (1 mg/kg) together with NDP-MSH (2 mg/kg; HY-N2466, MedChemExpress, United States); the LPS + NDP-MSH + H89 group received LPS (1 mg/kg), NDP-MSH (2 mg/kg), and the PKA inhibitor H89 (10 mg/kg; HY-15979A, MedChemExpress, United States); and the H89-alone group received H89 (10 mg/kg).

    Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Staining, Fluorescence, Activation Assay, Immunofluorescence

    NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .

    Journal: Frontiers in Pharmacology

    Article Title: NDP-MSH rescues LPS-induced neuroinflammation, synaptic deficits, and depressive-like behaviors in mice: involvement of MC1R–cAMP/PKA signaling

    doi: 10.3389/fphar.2026.1895800

    Figure Lengend Snippet: NDP-MSH Normalizes LPS-induced Metabolic Reprogramming through cAMP/PKA Signaling. (A) Principal component analysis (PCA) score plot of untargeted metabolomic profiles from saline control (CTRL), LPS-treated (LPS), drug-treated (NDP), drug plus inhibitor-treated (LNH), inhibitor alone (H89), and quality control (QC) samples. Biological samples included n = 4 mice per treatment group (CTRL, LPS, NDP, LNH, and H89). QC samples (n = 3) were used for quality control and were excluded from statistical comparisons. (B) Bar plot showing the number of significantly altered metabolites (upregulated and downregulated) across pairwise comparisons (limma, FDR <0.2, |log 2 fold change| ≥ 0.15; QC samples excluded). (C) Scatter plot showing the correlation between LPS-induced metabolic changes (LPS vs. CTRL) and drug-induced changes (NDP vs. LPS). (D) Scatter plot showing the correlation between drug-induced changes (NDP vs. LPS) and inhibitor-on-drug effects (LNH vs. NDP). (E) Heatmap showing a selected subset of metabolites whose LPS-induced changes were reversed by NDP-MSH treatment and whose NDP-MSH-mediated reversal was blocked by H89. Relative metabolite intensities were Z-score normalized across group means. (F) KEGG pathway enrichment analysis of drug-responsive metabolites. Source: BioRender.com .

    Article Snippet: Treatment regimens were as follows: vehicle-treated mice received equivalent volumes of saline; the LPS group received lipopolysaccharide (LPS; 1 mg/kg; L2880, Sigma-Aldrich, United States); the LPS + NDP-MSH group received LPS (1 mg/kg) together with NDP-MSH (2 mg/kg; HY-N2466, MedChemExpress, United States); the LPS + NDP-MSH + H89 group received LPS (1 mg/kg), NDP-MSH (2 mg/kg), and the PKA inhibitor H89 (10 mg/kg; HY-15979A, MedChemExpress, United States); and the H89-alone group received H89 (10 mg/kg).

    Techniques: Metabolomic, Saline, Control

    Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor H89 (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.

    Journal: European Journal of Histochemistry : EJH

    Article Title: Overexpression of GPER1 suppressed esophageal carcinoma growth via activating cAMP pathway

    doi: 10.4081/ejh.2026.4422

    Figure Lengend Snippet: Inhibition of the cAMP/PKA pathway attenuates GPER1-induced ferroptosis in esophageal cancer cells. KYSE70 and KYSE150 cells were treated with or without the cAMP/PKA inhibitor H89 (10 μM) for 24 h under four conditions: negative control with vehicle (NC + Veh), negative control with H89 (NC + H89), GPER1 overexpression with vehicle (GPER1-OE + Veh), and GPER1 overexpression with H89 (GPER1-OE + H89). a,d ) Cell viability was determined by CCK-8 assay in KYSE70 ( a ) and KYSE150 ( d ) cells. b,e ) Intracellular ROS levels were measured by flow cytometry using a DCFH-DA probe in KYSE70 ( b ) and KYSE150 ( e ) cells. c,f ) Intracellular Fe²⁺ content was quantified by an iron assay kit in KYSE70 ( c ) and KYSE150 ( f ) cells. g ) Protein expression levels of the ferroptosis markers ACSL4 and GPX4, and the cAMP pathway components p-CREB1 and CREB1, were analyzed by Western blotting in both KYSE70 and KYSE150 cells; left panels show representative Western blot images, and the right panels show the corresponding quantitative densitometric analysis of the protein bands, normalized to GAPDH (for ACSL4 and GPX4) or total CREB1 (for p-CREB1). All quantitative data are presented as the mean ±SD from three independent experiments (n=3). Statistical significance was determined by one-way ANOVA followed by Tukey's post-hoc test; * p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ns, not significant.

    Article Snippet: To functionally validate the role of the cAMP pathway in GPER1-induced ferroptosis, KYSE70 and KYSE150 cells with or without GPER1 overexpression were treated with the cAMP/PKA pathway inhibitor H89 (MedChemExpress, Monmouth Junction, NJ, USA).

    Techniques: Inhibition, Negative Control, Over Expression, CCK-8 Assay, Flow Cytometry, Iron Assay, Expressing, Western Blot