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<t>NDP-MSH</t> <t>ameliorates</t> LPS-induced inflammation-associated depressive-like behaviors and synaptic deficits, restores MC1R expression in the PFC. (A) Experimental timeline illustrating the LPS and NDP-MSH administration schedule and behavioral testing paradigm. (B) Sucrose preference in the SPT. NDP-MSH significantly reversed the LPS-induced reduction in sucrose preference (One-way ANOVA, F (2, 22) = 13.33, p < 0.001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 7.235, p < 0.001; LPS vs. LPS + NDP-MSH, q (22) = 4.576, p < 0.05; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (C) Representative locomotor traces in the OFT. (D) Total distance traveled in the OFT. NDP-MSH attenuated the LPS-induced reduction in total distance traveled (One-way ANOVA, F (2, 22) = 27.68, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 10.51, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.066, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (E) Number of center entries in the OFT. NDP-MSH significantly attenuated the LPS-induced reduction in center entries (One-way ANOVA, F (2, 22) = 24.18, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 9.831, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.283, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (F) Western blot analysis of MC1R protein expression in the PFC. NDP-MSH significantly increased MC1R protein levels in LPS-treated mice (One-way ANOVA, F (2, 6) = 5.477, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (6) = 2.605, p < 0.05; LPS vs. LPS + NDP-MSH, t (6) = 3.071, p < 0.05; n = 3 per group). All the values were normalized with loading control GAPDH. (G) Western blot and quantification showing significantly increased PSD95 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 8.682, p < 0.01, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.842, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 4.060, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (H) Western blot and quantification showing significantly increased GluA1 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 5.127, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.401, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 3.035, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (I) Western blot and quantification showing significantly increased pPKA protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2,24) = 2.628, p = 0.0929, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (24) = 0.1813, p = 0.8577; LPS vs. LPS + NDP-MSH, t (24) = 2.070, p < 0.05) (n = 9 per group). All the values were normalized with loading control GAPDH. Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Source: BioRender.com .

Ndp Msh, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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

NDP-MSH ameliorates LPS-induced inflammation-associated depressive-like behaviors and synaptic deficits, restores MC1R expression in the PFC. (A) Experimental timeline illustrating the LPS and NDP-MSH administration schedule and behavioral testing paradigm. (B) Sucrose preference in the SPT. NDP-MSH significantly reversed the LPS-induced reduction in sucrose preference (One-way ANOVA, F (2, 22) = 13.33, p < 0.001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 7.235, p < 0.001; LPS vs. LPS + NDP-MSH, q (22) = 4.576, p < 0.05; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (C) Representative locomotor traces in the OFT. (D) Total distance traveled in the OFT. NDP-MSH attenuated the LPS-induced reduction in total distance traveled (One-way ANOVA, F (2, 22) = 27.68, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 10.51, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.066, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (E) Number of center entries in the OFT. NDP-MSH significantly attenuated the LPS-induced reduction in center entries (One-way ANOVA, F (2, 22) = 24.18, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 9.831, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.283, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (F) Western blot analysis of MC1R protein expression in the PFC. NDP-MSH significantly increased MC1R protein levels in LPS-treated mice (One-way ANOVA, F (2, 6) = 5.477, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (6) = 2.605, p < 0.05; LPS vs. LPS + NDP-MSH, t (6) = 3.071, p < 0.05; n = 3 per group). All the values were normalized with loading control GAPDH. (G) Western blot and quantification showing significantly increased PSD95 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 8.682, p < 0.01, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.842, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 4.060, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (H) Western blot and quantification showing significantly increased GluA1 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 5.127, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.401, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 3.035, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (I) Western blot and quantification showing significantly increased pPKA protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2,24) = 2.628, p = 0.0929, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (24) = 0.1813, p = 0.8577; LPS vs. LPS + NDP-MSH, t (24) = 2.070, p < 0.05) (n = 9 per group). All the values were normalized with loading control GAPDH. Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Source: BioRender.com .

Figure Legend Snippet: NDP-MSH ameliorates LPS-induced inflammation-associated depressive-like behaviors and synaptic deficits, restores MC1R expression in the PFC. (A) Experimental timeline illustrating the LPS and NDP-MSH administration schedule and behavioral testing paradigm. (B) Sucrose preference in the SPT. NDP-MSH significantly reversed the LPS-induced reduction in sucrose preference (One-way ANOVA, F (2, 22) = 13.33, p < 0.001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 7.235, p < 0.001; LPS vs. LPS + NDP-MSH, q (22) = 4.576, p < 0.05; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (C) Representative locomotor traces in the OFT. (D) Total distance traveled in the OFT. NDP-MSH attenuated the LPS-induced reduction in total distance traveled (One-way ANOVA, F (2, 22) = 27.68, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 10.51, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.066, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (E) Number of center entries in the OFT. NDP-MSH significantly attenuated the LPS-induced reduction in center entries (One-way ANOVA, F (2, 22) = 24.18, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 9.831, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.283, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (F) Western blot analysis of MC1R protein expression in the PFC. NDP-MSH significantly increased MC1R protein levels in LPS-treated mice (One-way ANOVA, F (2, 6) = 5.477, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (6) = 2.605, p < 0.05; LPS vs. LPS + NDP-MSH, t (6) = 3.071, p < 0.05; n = 3 per group). All the values were normalized with loading control GAPDH. (G) Western blot and quantification showing significantly increased PSD95 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 8.682, p < 0.01, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.842, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 4.060, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (H) Western blot and quantification showing significantly increased GluA1 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 5.127, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.401, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 3.035, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (I) Western blot and quantification showing significantly increased pPKA protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2,24) = 2.628, p = 0.0929, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (24) = 0.1813, p = 0.8577; LPS vs. LPS + NDP-MSH, t (24) = 2.070, p < 0.05) (n = 9 per group). All the values were normalized with loading control GAPDH. Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Source: BioRender.com .

Techniques Used: Expressing, Western Blot, Control

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

MC1R activation enhances synaptic transmission and intrinsic excitability in PFC neurons. (A) Representative traces of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from mPFC pyramidal neurons. (B) Quantification of the frequency of sEPSCs in neurons from Vehicle- and NDP-MSH-treated mice. NDP-MSH significantly increased sEPSC frequency (two-tailed unpaired Student’s t-test, T 21 = 2.473, p < 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (C) Quantification of sEPSC amplitude showing no significant difference between Vehicle and NDP-MSH groups (two-tailed unpaired Student’s t-test, T 21 = 0.1817, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (D) Comparison of input resistance (MΩ) between Vehicle- and NDP-MSH–treated neurons, with no significant change observed (two-tailed unpaired Student’s t-test, T 21 = 0.6470, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (E) Representative traces showing rheobase-evoked action potentials in neurons from Vehicle-treated (left) and NDP-MSH–treated (right) groups. The minimal current injection step (Δ5 pA, 30 ms) required to evoke the first spike is indicated, with corresponding rheobase currents and resting membrane potentials shown below traces. (F) Summary of resting membrane potential (RMP) in Vehicle and NDP-MSH groups. No significant difference was observed between groups (two-tailed unpaired Student’s t-test, T 21 = 1.986, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (G) Quantification of rheobase current showing comparable current thresholds for action potential initiation between Vehicle- and NDP-MSH–treated neurons (two-tailed unpaired Student’s t-test, T 21 = 0.8929, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (H) Representative current-clamp recordings showing action potentials evoked by a 100 pA current step in neurons from Vehicle-treated and NDP-MSH-treated groups. Neurons exposed to NDP-MSH displayed increased spike firing under the same current injection. (I) Frequency-current (F–I) relationship showing evoked spike numbers in response to increasing depolarizing current injections in Vehicle and NDP-MSH groups. Two-way repeated-measures ANOVA revealed a significant Current × Treatment interaction (F (8, 168) = 3.600, p < 0.001) and a significant main effect of treatment (F (1, 21) = 7.456, p < 0.05), indicating that NDP-MSH increased spike output compared with Vehicle. Šídák’s multiple comparisons test showed significant differences between Vehicle and NDP-MSH groups at the indicated current intensities (* p < 0.05, ** p < 0.01) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01. Source: BioRender.com .

Figure Legend Snippet: MC1R activation enhances synaptic transmission and intrinsic excitability in PFC neurons. (A) Representative traces of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from mPFC pyramidal neurons. (B) Quantification of the frequency of sEPSCs in neurons from Vehicle- and NDP-MSH-treated mice. NDP-MSH significantly increased sEPSC frequency (two-tailed unpaired Student’s t-test, T 21 = 2.473, p < 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (C) Quantification of sEPSC amplitude showing no significant difference between Vehicle and NDP-MSH groups (two-tailed unpaired Student’s t-test, T 21 = 0.1817, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (D) Comparison of input resistance (MΩ) between Vehicle- and NDP-MSH–treated neurons, with no significant change observed (two-tailed unpaired Student’s t-test, T 21 = 0.6470, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (E) Representative traces showing rheobase-evoked action potentials in neurons from Vehicle-treated (left) and NDP-MSH–treated (right) groups. The minimal current injection step (Δ5 pA, 30 ms) required to evoke the first spike is indicated, with corresponding rheobase currents and resting membrane potentials shown below traces. (F) Summary of resting membrane potential (RMP) in Vehicle and NDP-MSH groups. No significant difference was observed between groups (two-tailed unpaired Student’s t-test, T 21 = 1.986, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (G) Quantification of rheobase current showing comparable current thresholds for action potential initiation between Vehicle- and NDP-MSH–treated neurons (two-tailed unpaired Student’s t-test, T 21 = 0.8929, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (H) Representative current-clamp recordings showing action potentials evoked by a 100 pA current step in neurons from Vehicle-treated and NDP-MSH-treated groups. Neurons exposed to NDP-MSH displayed increased spike firing under the same current injection. (I) Frequency-current (F–I) relationship showing evoked spike numbers in response to increasing depolarizing current injections in Vehicle and NDP-MSH groups. Two-way repeated-measures ANOVA revealed a significant Current × Treatment interaction (F (8, 168) = 3.600, p < 0.001) and a significant main effect of treatment (F (1, 21) = 7.456, p < 0.05), indicating that NDP-MSH increased spike output compared with Vehicle. Šídák’s multiple comparisons test showed significant differences between Vehicle and NDP-MSH groups at the indicated current intensities (* p < 0.05, ** p < 0.01) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01. Source: BioRender.com .

Techniques Used: Activation Assay, Transmission Assay, Two Tailed Test, Comparison, Injection, Membrane

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

Sonication:

Article Title: Engineered Macrophage Membrane-Coated Nanoparticles for Hepatic Ischemia–Reperfusion Injury Therapeutics
Article Snippet: .. Briefly, PLGA (50 mg/ml, 1 ml, Daigangbio) in dichloromethane with MT (2 mg/ml, 1 ml, MCE) was added to 5% w/v PVA (RHAWN) solution by sonication (42 kHz, 100 W) for 5 min in ice bath conditions to obtain an emulsion. ..

Emulsion:

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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 ameliorates LPS-induced inflammation-associated depressive-like behaviors and synaptic deficits, restores MC1R expression in the PFC. (A) Experimental timeline illustrating the LPS and NDP-MSH administration schedule and behavioral testing paradigm. (B) Sucrose preference in the SPT. NDP-MSH significantly reversed the LPS-induced reduction in sucrose preference (One-way ANOVA, F (2, 22) = 13.33, p < 0.001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 7.235, p < 0.001; LPS vs. LPS + NDP-MSH, q (22) = 4.576, p < 0.05; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (C) Representative locomotor traces in the OFT. (D) Total distance traveled in the OFT. NDP-MSH attenuated the LPS-induced reduction in total distance traveled (One-way ANOVA, F (2, 22) = 27.68, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 10.51, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.066, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (E) Number of center entries in the OFT. NDP-MSH significantly attenuated the LPS-induced reduction in center entries (One-way ANOVA, F (2, 22) = 24.18, p < 0.0001, followed by Tukey’s multiple comparisons test. Vehicle vs. LPS, q (22) = 9.831, p < 0.0001; LPS vs. LPS + NDP-MSH, q (22) = 5.283, p < 0.01; Vehicle, n = 9; LPS, n = 8; LPS + NDP-MSH, n = 8). (F) Western blot analysis of MC1R protein expression in the PFC. NDP-MSH significantly increased MC1R protein levels in LPS-treated mice (One-way ANOVA, F (2, 6) = 5.477, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (6) = 2.605, p < 0.05; LPS vs. LPS + NDP-MSH, t (6) = 3.071, p < 0.05; n = 3 per group). All the values were normalized with loading control GAPDH. (G) Western blot and quantification showing significantly increased PSD95 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 8.682, p < 0.01, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.842, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 4.060, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (H) Western blot and quantification showing significantly increased GluA1 protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2, 15) = 5.127, p < 0.05, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (15) = 2.401, p < 0.05; LPS vs. LPS + NDP-MSH, t (15) = 3.035, p < 0.01; n = 6 per group). All the values were normalized with loading control GAPDH. (I) Western blot and quantification showing significantly increased pPKA protein levels in the NDP-MSH group compared with the LPS group (One-way ANOVA, F (2,24) = 2.628, p = 0.0929, followed by Fisher’s LSD test for planned pairwise comparisons. Vehicle vs. LPS, t (24) = 0.1813, p = 0.8577; LPS vs. LPS + NDP-MSH, t (24) = 2.070, p < 0.05) (n = 9 per group). All the values were normalized with loading control GAPDH. Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Source: BioRender.com .

Article Snippet: NDP-MSH (HY-N2466, MedChemExpress, United States) was dissolved in double-distilled water to prepare a stock solution (5 μg/μL), aliquoted, and stored at −20 °C.

Techniques: Expressing, Western Blot, Control

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: NDP-MSH (HY-N2466, MedChemExpress, United States) was dissolved in double-distilled water to prepare a stock solution (5 μg/μL), aliquoted, and stored at −20 °C.

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

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: MC1R activation enhances synaptic transmission and intrinsic excitability in PFC neurons. (A) Representative traces of spontaneous excitatory postsynaptic currents (sEPSCs) recorded from mPFC pyramidal neurons. (B) Quantification of the frequency of sEPSCs in neurons from Vehicle- and NDP-MSH-treated mice. NDP-MSH significantly increased sEPSC frequency (two-tailed unpaired Student’s t-test, T 21 = 2.473, p < 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (C) Quantification of sEPSC amplitude showing no significant difference between Vehicle and NDP-MSH groups (two-tailed unpaired Student’s t-test, T 21 = 0.1817, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (D) Comparison of input resistance (MΩ) between Vehicle- and NDP-MSH–treated neurons, with no significant change observed (two-tailed unpaired Student’s t-test, T 21 = 0.6470, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (E) Representative traces showing rheobase-evoked action potentials in neurons from Vehicle-treated (left) and NDP-MSH–treated (right) groups. The minimal current injection step (Δ5 pA, 30 ms) required to evoke the first spike is indicated, with corresponding rheobase currents and resting membrane potentials shown below traces. (F) Summary of resting membrane potential (RMP) in Vehicle and NDP-MSH groups. No significant difference was observed between groups (two-tailed unpaired Student’s t-test, T 21 = 1.986, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (G) Quantification of rheobase current showing comparable current thresholds for action potential initiation between Vehicle- and NDP-MSH–treated neurons (two-tailed unpaired Student’s t-test, T 21 = 0.8929, p > 0.05) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). (H) Representative current-clamp recordings showing action potentials evoked by a 100 pA current step in neurons from Vehicle-treated and NDP-MSH-treated groups. Neurons exposed to NDP-MSH displayed increased spike firing under the same current injection. (I) Frequency-current (F–I) relationship showing evoked spike numbers in response to increasing depolarizing current injections in Vehicle and NDP-MSH groups. Two-way repeated-measures ANOVA revealed a significant Current × Treatment interaction (F (8, 168) = 3.600, p < 0.001) and a significant main effect of treatment (F (1, 21) = 7.456, p < 0.05), indicating that NDP-MSH increased spike output compared with Vehicle. Šídák’s multiple comparisons test showed significant differences between Vehicle and NDP-MSH groups at the indicated current intensities (* p < 0.05, ** p < 0.01) (Vehicle, n = 11 neurons; NDP-MSH, n = 12 neurons). Data are presented as mean ± SEM. Statistical significance: * p < 0.05, ** p < 0.01. Source: BioRender.com .

Article Snippet: NDP-MSH (HY-N2466, MedChemExpress, United States) was dissolved in double-distilled water to prepare a stock solution (5 μg/μL), aliquoted, and stored at −20 °C.

Techniques: Activation Assay, Transmission Assay, Two Tailed Test, Comparison, Injection, Membrane

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: NDP-MSH (HY-N2466, MedChemExpress, United States) was dissolved in double-distilled water to prepare a stock solution (5 μg/μL), aliquoted, and stored at −20 °C.

Techniques: Metabolomic, Saline, Control

Description of the included systematic reviews; number of original studies included, population, intervention and control. Motor Control Exercises (MCE)

Journal: BMC Musculoskeletal Disorders

Article Title: Summarizing the effects of different exercise types in chronic low back pain – a systematic review of systematic reviews

doi: 10.1186/s12891-022-05722-x

Figure Lengend Snippet: Description of the included systematic reviews; number of original studies included, population, intervention and control. Motor Control Exercises (MCE)

Article Snippet: Macedo et al. (2009) [ ] AMSTAR-2 Moderate , Pain: VAS Disability: ODI Follow up: Short term: ≤ 3 mo Intermediate term: > 3 and < 12 mo Long term: ≥ 12 mo , MCE = GE All time intervals Short term (4 trials) Intermediate (3 trials) Long term (3 trials) MCE > MT Intermediate (4 trials) WMD = -5.7 (95%CI -10.7; -0.8) MCE > MI Short-term (7 trials) WMD = -14.3 (95%CI -20.4; -8.1) Intermediate (7 trials) WMD = -13.6 (95%CI -22.4; -4.1) Long-term (7 trials) WMD = -14.4 (95%CI -23.1; -5.7) , MCE > GE Short-term (5 trials) WMD = -5.1 (95%CI -8.7; -1.4) MCE > MT Intermediate (4 trials) WMD = -4.0 (95%CI -7.6; -0.4) MCE > MI Long-term (7 trials) WMD = -10.8 95%CI (-18.7; -2.8) , MCE is more effective than MI and add benefit to another form of intervention in reducing pain and disability in LBP. The optimal implementation of MCE is unclear. Future trials need to study dosage parameters, feedback and subgroups..

Techniques: Control, Muscles, Isolation, Functional Assay, Activity Assay

Results of different exercise types compared to control interventions for pain and disability. Motor Control Exercises (MCE)

Journal: BMC Musculoskeletal Disorders

Article Title: Summarizing the effects of different exercise types in chronic low back pain – a systematic review of systematic reviews

doi: 10.1186/s12891-022-05722-x

Figure Lengend Snippet: Results of different exercise types compared to control interventions for pain and disability. Motor Control Exercises (MCE)

Techniques: Control, Activation Assay

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