Journal: Journal of Neuroscience

Article Title: Distinctive Features of Adult Ocular Dominance Plasticity

doi: 10.1523/jneurosci.2451-08.2008

Figure Lengend Snippet: Figure 4. CPP-mediated suppression of NMDA receptor function in visual cortex and NMDA receptor-dependent ocular dom- inanceplasticityinthecriticalperiod.A,SuppressionofZif268expressioninvisualcortexat24hafterCPPinjectioninjuvenileand adultmice.CPPorcontrolsaline(Cont)wereinjectedintomiceinthecriticalperiodatP28andinadulthoodatP80andtheamount ofzif268(top)andIIItubulin(bottom)proteinsat24hafterinjectionwasquantifiedbyimmunoblotting.Therightpanelshows summarydata(n3each;*p0.05,**p0.01).B,MiceinthecriticalperiodweretreatedwithCPP4–6hbeforeMDonday 0 and every 24 h thereafter and were imaged at 4 d after MD. C, OD shifts after 4 d MD were blocked by daily CPP treatment in critical period mice (n 3–6; *p 0.05, **p 0.01). Data indicated in open circles were taken from Figure 1 for comparison. D, Decrease in the response of the deprived eye after 4 d MD was prevented by daily CPP treatment in critical period mice (n 3–6).E,PolarmapsofcorticalresponsesofcriticalperiodmicewithorwithoutCPPtreatmentandMD.Contra,Contralateral;Ipsi, ipsilateral.

Article Snippet: The competitive NMDA receptor antagonist ( R, S)-3(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid (CPP) (Tocris Bioscience) was dissolved in saline at a concentration of 1–1.5 mg/ml and the drug solution was injected intraperitoneally at a dose of 10 –15 mg/kg every 24 h (Villarreal et al., 2002).

Techniques: Comparison

Journal: International journal of molecular medicine

Article Title: Naringenin modulates the NO‑cGMP‑PKG signaling pathway by binding to AKT to enhance osteogenic differentiation in hPDLSCs.

doi: 10.3892/ijmm.2024.5391

Figure Lengend Snippet: Figure 2. Volcano plot, clustered heatmap, KEGG analysis and validation of the expression of associated factors. (A) Volcano plot depicting the differential gene expression between the NAR and control groups. (B) Heatmap illustrating the gene expression differences between the NAR and control groups. (C) Kyoto Encyclopedia of Genes and Genomes analysis of differentially expressed genes between the NAR and control groups. (D) ELISA detection of cGMP production. (E) Reverse transcription‑quantitative PCR‑based detection of TRPC6, PKG and sGC expression. (F and G) Protein expression analysis of PKG, TRPC6 and sGC. *P<0.05, **P<0.01. NAR, naringenin; cGMP, cyclic guanosine monophosphate; TRPC6, transient receptor potential cation channel, subfamily C, member 6; PKG, protein kinase G; sGC, soluble guanylate cyclase.

Article Snippet: Cells treated with NAR (10 μmol/l) were also treated with NG‐nitro‐L‐arginine methyl ester (L‐NAME; 70 μM) to inhibit endothelial nitric oxide synthase (eNOS), 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 20 μM) to inhibit soluble guanylate cyclase (sGC) and AKT inhibitor VIII (58 nM) to inhibit AKT, as recommended by the manufacturer (MedChemExpress for all).

Techniques: Biomarker Discovery, Expressing, Gene Expression, Control, Enzyme-linked Immunosorbent Assay

Journal: International journal of molecular medicine

Article Title: Naringenin modulates the NO‑cGMP‑PKG signaling pathway by binding to AKT to enhance osteogenic differentiation in hPDLSCs.

doi: 10.3892/ijmm.2024.5391

Figure Lengend Snippet: Figure 3. Ability of NAR to promote osteogenesis in human periodontal ligament stem cells is mitigated after L‑NAME (eNOS inhibitor) treatment. (A) Alkaline phosphatase staining in different treatment groups. (B) Alizarin red staining in different treatment groups. (C) NO levels in different treatment groups. (D) Gene expression levels of RUNX2, OPN and sGC in different treatment groups. (E‑G) Protein expression of RUNX2, OPN, sGC and p‑eNOS in various treatment groups. *P<0.05, **P<0.01, ***P<0.001. NAR, naringenin; eNOS, endothelial nitric oxide synthase; RUNX2, Runt‑related transcription factor; OPN, osteopontin; sGC, soluble guanylate cyclase; NO, nitric oxide; p‑, phosphorylated; t‑, total; L‑NAME, NG‑nitro‑L‑arginine methyl ester.

Article Snippet: Cells treated with NAR (10 μmol/l) were also treated with NG‐nitro‐L‐arginine methyl ester (L‐NAME; 70 μM) to inhibit endothelial nitric oxide synthase (eNOS), 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 20 μM) to inhibit soluble guanylate cyclase (sGC) and AKT inhibitor VIII (58 nM) to inhibit AKT, as recommended by the manufacturer (MedChemExpress for all).

Techniques: Staining, Gene Expression, Expressing

Journal: International journal of molecular medicine

Article Title: Naringenin modulates the NO‑cGMP‑PKG signaling pathway by binding to AKT to enhance osteogenic differentiation in hPDLSCs.

doi: 10.3892/ijmm.2024.5391

Figure Lengend Snippet: Figure 4. Ability of NAR to promote osteogenesis in human periodontal ligament stem cells is decreased after ODQ (an sGC inhibitor) treatment. (A) Alkaline phosphatase staining in different treatment groups. (B) Alizarin red staining in different treatment groups. (C) cGMP expression in different treatment groups. (D and E) Gene expression levels of RUNX2, OPN, sGC, PKG and TRPC6 in different treatment groups. (F‑H) Protein levels of RUNX2, OPN, sGC, PKG and TRPC6 in different treatment groups. *P<0.05, **P<0.01, ***P<0.001. NAR, naringenin; cGMP, cyclic guanosine monophosphate; sGC, soluble guanylate cyclase; RUNX2, Runt‑related transcription factor; OPN, osteopontin; TRPC6, transient receptor potential cation channel, subfamily C, member 6; PKG, protein kinase G; ODQ, 1H‑[1,2,4]oxadiazolo[4,3‑a]quinoxalin‑1‑one.

Article Snippet: Cells treated with NAR (10 μmol/l) were also treated with NG‐nitro‐L‐arginine methyl ester (L‐NAME; 70 μM) to inhibit endothelial nitric oxide synthase (eNOS), 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 20 μM) to inhibit soluble guanylate cyclase (sGC) and AKT inhibitor VIII (58 nM) to inhibit AKT, as recommended by the manufacturer (MedChemExpress for all).

Techniques: Staining, Expressing, Gene Expression

Journal: International journal of molecular medicine

Article Title: Naringenin modulates the NO‑cGMP‑PKG signaling pathway by binding to AKT to enhance osteogenic differentiation in hPDLSCs.

doi: 10.3892/ijmm.2024.5391

Figure Lengend Snippet: Figure 8. Schematic diagram of the mechanism by which naringenin promotes the osteogenic differentiation of human periodontal ligament stem cells. eNOS, endothelial nitric oxide synthase; p, phosphorylated; NO, nitric oxide; sGC, soluble guanylate cyclase; cGMP, cyclic guanosine monophosphate; TRPC6, transient receptor potential cation channel, subfamily C, member 6; PKG, protein kinase G.

Article Snippet: Cells treated with NAR (10 μmol/l) were also treated with NG‐nitro‐L‐arginine methyl ester (L‐NAME; 70 μM) to inhibit endothelial nitric oxide synthase (eNOS), 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxalin‐1‐one (ODQ; 20 μM) to inhibit soluble guanylate cyclase (sGC) and AKT inhibitor VIII (58 nM) to inhibit AKT, as recommended by the manufacturer (MedChemExpress for all).

Techniques: