Review



pka inhibitor h89  (MedChemExpress)


Bioz Verified Symbol MedChemExpress is a verified supplier
Bioz Manufacturer Symbol MedChemExpress manufactures this product  
  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 97

    Structured Review

    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+h+89/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

    other:

    Article Title: The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner.
    Article Snippet: The PKA inhibitor H-89 and the Epac2 inhibitor ESI-09 were purchased from MedChemExpress (New Jersey, USA) and Cayman Chemical (Michigan, USA), respectively.

    Article Title: The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner.
    Article Snippet: Total RNA was isolated from pancreatic islets and the hypothalamus using an RNase-free DNase and RNeasy Kit (Qiagen, Valencia, CA). cDNA was prepared using high-capacity cDNA reverse-transcription kits (Applied Biosystems).

    Article Title: The matricellular protein Fibulin-5 regulates β-cell proliferation in an autocrine/paracrine manner
    Article Snippet: The PKA inhibitor H-89 and the Epac2 inhibitor ESI-09 were purchased from MedChemExpress (New Jersey, USA) and Cayman Chemical (Michigan, USA), respectively.

    Cell Culture:

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway
    Article Snippet: In short, cells were cultured with RPMI 1640 (Thermo, Cat# 11879020) 738 without glucose and FBS in a 95% N2 and 5% CO2 chamber for two hours. .. After hypoxia, the RPMI 1640 739 was replaced with DMEM and cultured in a 95% air and 5% CO2 incubator for 24 h. While performing 740 reoxygenation, the following medications were added: non-selective β-AR blocker propranolol (10 μM, 741 Sigma-Aldrich, Cat# 40543), non-selective β-AR agonist isoproterenol (10 μM, Sigma-Aldrich, Cat# 742 16504), β1-AR agonist dobutamine (0.5 μM, MCE, Cat# HY-15746A), β1-AR blocker betaxolol (0.3 μM, 743 MCE, Cat# HY-B0381), β2-AR agonist salmeterol (0.5 μM, MCE, Cat# HY-14302), β2-AR blocker 744 ICI118,551 (0.3 μM, MCE, Cat# HY-13951), PKA inhibitor H-89 (10 μM, MCE, Cat# HY-15979A), ERK 745 inhibitor U0126 (10 μM, MCE, Cat# HY-12031A) and vehicle. ..

    Medications:

    Article Title: Propranolol alleviates cerebral infarction through the β2-AR-mediated ERK/NLRP3 pathway
    Article Snippet: In short, cells were cultured with RPMI 1640 (Thermo, Cat# 11879020) 738 without glucose and FBS in a 95% N2 and 5% CO2 chamber for two hours. .. After hypoxia, the RPMI 1640 739 was replaced with DMEM and cultured in a 95% air and 5% CO2 incubator for 24 h. While performing 740 reoxygenation, the following medications were added: non-selective β-AR blocker propranolol (10 μM, 741 Sigma-Aldrich, Cat# 40543), non-selective β-AR agonist isoproterenol (10 μM, Sigma-Aldrich, Cat# 742 16504), β1-AR agonist dobutamine (0.5 μM, MCE, Cat# HY-15746A), β1-AR blocker betaxolol (0.3 μM, 743 MCE, Cat# HY-B0381), β2-AR agonist salmeterol (0.5 μM, MCE, Cat# HY-14302), β2-AR blocker 744 ICI118,551 (0.3 μM, MCE, Cat# HY-13951), PKA inhibitor H-89 (10 μM, MCE, Cat# HY-15979A), ERK 745 inhibitor U0126 (10 μM, MCE, Cat# HY-12031A) and vehicle. ..

    Incubation:

    Article Title: Photobiomodulation therapy at 632 nm wavelength ameliorates intrauterine adhesion via activation of cAMP/PKA/CREB pathway.
    Article Snippet: Intrauterine adhesion (IUA), or Asherman's syndrome, has the pathological characterization of a completely or partially blocked uterine cavity caused by endometrial fibrosis, mainly resulting from endometrial injury or infection.1 IUA is the most common cause of secondary infertility in females and can lead to other problems in the reproductive system, such as hypomenorrhea, amenorrhea, and recurrent abortion.1 Therefore, uterine cavity Received: 13 February 2023 | Revised: 3 May 2023 | Accepted: 4 May 2023 DOI: 10.1111/php.13813



    Similar Products

    97
    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 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+h+89/H-89/pmc13487505-47-58-64
    Average 97 stars, based on 1 article reviews
    pka inhibitor h89 - by Bioz Stars, 2026-09
    97/100 stars
      Buy from Supplier

    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
    https://www.bioz.com/product/pka+inhibitor+h+89/H-89/pm41988986-311-36-43
    Average 97 stars, based on 1 article reviews
    prka pka inhibitor h89 - by Bioz Stars, 2026-09
    97/100 stars
      Buy from Supplier

    95
    MedChemExpress pka inhibitor h 89
    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 H 89, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+h+89/H-89/10__1016_slash_j__isci__2026__115779-734-86-91
    Average 95 stars, based on 1 article reviews
    pka inhibitor h 89 - by Bioz Stars, 2026-09
    95/100 stars
      Buy from Supplier

    95
    Selleck Chemicals pka inhibitor
    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, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+h+89/H+89+2HCl/pm41876468-194-1-16
    Average 95 stars, based on 1 article reviews
    pka inhibitor - by Bioz Stars, 2026-09
    95/100 stars
      Buy from Supplier

    95
    Selleck Chemicals pka inhibitor h 89 2hcl
    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 H 89 2hcl, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/pka+inhibitor+h+89/H+89+2HCl/pm41805786-300-55-63
    Average 95 stars, based on 1 article reviews
    pka inhibitor h 89 2hcl - by Bioz Stars, 2026-09
    95/100 stars
      Buy from Supplier

    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