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pd90780  (MedChemExpress)


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    Structured Review

    MedChemExpress pd90780
    Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), <t>PD90780</t> (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Pd90780, 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
    https://www.bioz.com/result/pd90780/product/MedChemExpress
    Average 94 stars, based on 2 article reviews
    pd90780 - by Bioz Stars, 2026-02
    94/100 stars

    Images

    1) Product Images from "Astragaloside II, a natural saponin, facilitates remyelination in demyelination neurological diseases via p75NTR receptor mediated β-catenin/Id2/MBP signaling axis in oligodendrocyte precursor cells"

    Article Title: Astragaloside II, a natural saponin, facilitates remyelination in demyelination neurological diseases via p75NTR receptor mediated β-catenin/Id2/MBP signaling axis in oligodendrocyte precursor cells

    Journal: Journal of Advanced Research

    doi: 10.1016/j.jare.2025.04.028

    Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), PD90780 (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Figure Legend Snippet: Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), PD90780 (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Techniques Used: Staining, Sequencing, Binding Assay, SPR Assay, Expressing, Transfection, Mutagenesis



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    Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), <t>PD90780</t> (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
    Pd90780, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), <t>PD90780</t> (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Axon Medchem LLC p75ntr blocker pd90780
    Effects of TrkA and p75 NTR blocker treatments on bile duct ligation (BDL)-induced mouse liver injury. The ICR mice receiving BDL surgery were intraperitoneally administered either recombinant NGF ( n =6) twice weekly or PBS ( n =6), GW441756 (GW; n =6), DMSO ( n =3) or <t>PD90780</t> (PD; n =6) daily. At 14 days postoperation, serum levels of AST ( a ), ALT ( b ) and total bilirubin ( c ) were biochemically measured, whereas tumor necrosis factor (TNF)-α ( d ) and interleukin (IL)-6 ( e ) levels in serum were analyzed by ELISA. The H&E staining results of mice with BDL-induced cholestatic injury or simultaneous treatments show the hepatic necrotic regions in dashed circles ( f ), quantified by morphometric analysis ( g ). Scale bar=1000 μm. All of the data are shown as the mean±s.e.m. ND, not detectable. NS, not significant. * P <0.05 between the indicated groups.
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    Image Search Results


    Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), PD90780 (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: Journal of Advanced Research

    Article Title: Astragaloside II, a natural saponin, facilitates remyelination in demyelination neurological diseases via p75NTR receptor mediated β-catenin/Id2/MBP signaling axis in oligodendrocyte precursor cells

    doi: 10.1016/j.jare.2025.04.028

    Figure Lengend Snippet: Affinity studies between AS-II and its target p75NTR . (A, B) Coomassie Blue staining and MS-based DARTs sequencing were conducted to identify the target proteins of AS-II. (C) Molecular docking visualization of AS-II binding to p75NTR complex structure. (D) Molecular docking results for p75NTR (PDB: 5ZGG) with AS-II, NSC49652, and K252a. (E) Antiproteolytic effect of p75NTR protein in combination with AS-II (n = 4). (F) Effects of varying concentrations of AS-II on its binding and protease resistance to p75NTR (n = 4). (G) Thermal stability of p75NTR with or without AS-II (n = 4). (H) Binding affinities of AS-II and K252a (at concentrations from 1.5625-100 μM), PD90780 (at concentrations from 1.5625-200 μM) to p75NTR were determined using SPR assay. (I) Predicted binding sites of AS-II to p75NTR. (J) Effects of AS-II (100 μM) on the expression of GSK3β Tyr216 , β-catenin, and MBP in MO3.13 cells transfected with WT or mutant p75NTR (n = 4). Data are presented as mean ± SD; & p < 0.05, && p < 0.01, vs GAPDH band; # p < 0.05, ### p < 0.001, vs Ctrl group; * p < 0.05, ** p < 0.01, vs DMSO group. ns, not significant. Statistical test: Two-group comparisons used Student's t -test (E, G, J), multi-group comparisons used one-way ANOVA with Dunnett's test (F). (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: 3,3′,5-Triiodo-L-thyronine (T3, Cat. No. HY-A0070), SKL2001 (Cat. No. HY-101085), PD90780 (Cat. No. HY-110166 ), and K252a (Cat. No. HY-N6732) were obtained from MedChemExpress (Monmouth Junction, NJ, USA).

    Techniques: Staining, Sequencing, Binding Assay, SPR Assay, Expressing, Transfection, Mutagenesis

    Effects of TrkA and p75 NTR blocker treatments on bile duct ligation (BDL)-induced mouse liver injury. The ICR mice receiving BDL surgery were intraperitoneally administered either recombinant NGF ( n =6) twice weekly or PBS ( n =6), GW441756 (GW; n =6), DMSO ( n =3) or PD90780 (PD; n =6) daily. At 14 days postoperation, serum levels of AST ( a ), ALT ( b ) and total bilirubin ( c ) were biochemically measured, whereas tumor necrosis factor (TNF)-α ( d ) and interleukin (IL)-6 ( e ) levels in serum were analyzed by ELISA. The H&E staining results of mice with BDL-induced cholestatic injury or simultaneous treatments show the hepatic necrotic regions in dashed circles ( f ), quantified by morphometric analysis ( g ). Scale bar=1000 μm. All of the data are shown as the mean±s.e.m. ND, not detectable. NS, not significant. * P <0.05 between the indicated groups.

    Journal: Experimental & Molecular Medicine

    Article Title: Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

    doi: 10.1038/emm.2017.235

    Figure Lengend Snippet: Effects of TrkA and p75 NTR blocker treatments on bile duct ligation (BDL)-induced mouse liver injury. The ICR mice receiving BDL surgery were intraperitoneally administered either recombinant NGF ( n =6) twice weekly or PBS ( n =6), GW441756 (GW; n =6), DMSO ( n =3) or PD90780 (PD; n =6) daily. At 14 days postoperation, serum levels of AST ( a ), ALT ( b ) and total bilirubin ( c ) were biochemically measured, whereas tumor necrosis factor (TNF)-α ( d ) and interleukin (IL)-6 ( e ) levels in serum were analyzed by ELISA. The H&E staining results of mice with BDL-induced cholestatic injury or simultaneous treatments show the hepatic necrotic regions in dashed circles ( f ), quantified by morphometric analysis ( g ). Scale bar=1000 μm. All of the data are shown as the mean±s.e.m. ND, not detectable. NS, not significant. * P <0.05 between the indicated groups.

    Article Snippet: A p75NTR blocker, PD90780, was purchased from Axon Medchem (Groningen, The Netherlands).

    Techniques: Ligation, Recombinant, Enzyme-linked Immunosorbent Assay, Staining

    Effects of TrkA and p75 NTR blocker treatments on bile duct ligation (BDL)-induced PARP cleavage and apoptosis of parenchymal hepatocytes. The mice receiving BDL surgery were intraperitoneally administered with either recombinant NGF ( n =6) twice weekly or PBS ( n =6), GW441756 (GW; n =6), DMSO ( n =3) or PD90780 (PD; n =6) daily. After 2 weeks of treatment, pooled liver extracts of each group were subjected to western blotting to detect both propeptides and cleaved forms of caspase-3 and PARP ( a ). Density analysis of the activation of caspase-3 ( b ) and PARP ( c ), shown as the ratios of cleavage to propeptide content, followed by normalization to negative control (NC) levels. IHC staining for active PARP peptides ( d ) and labeling index ( e ) quantitatively demonstrated that PD90780 administration potentiated the increase of PARP activation in BDL-treated mouse livers. ( f ) Representative microphotographs of TUNEL staining showing the apoptotic events in mouse liver sections. Scale bars=50 μm. ( g ) Analysis of TUNEL-positive parenchymal cells indicated that recombinant NGF administration exerted a protective effect, whereas treatment with a p75NTR antagonist, PD90780, increased apoptotic cell death in BDL-induced cholestatic injured livers. All data are shown as the mean±s.e.m. * P <0.05 between indicated groups. ND, not detectable. NS, not significant.

    Journal: Experimental & Molecular Medicine

    Article Title: Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

    doi: 10.1038/emm.2017.235

    Figure Lengend Snippet: Effects of TrkA and p75 NTR blocker treatments on bile duct ligation (BDL)-induced PARP cleavage and apoptosis of parenchymal hepatocytes. The mice receiving BDL surgery were intraperitoneally administered with either recombinant NGF ( n =6) twice weekly or PBS ( n =6), GW441756 (GW; n =6), DMSO ( n =3) or PD90780 (PD; n =6) daily. After 2 weeks of treatment, pooled liver extracts of each group were subjected to western blotting to detect both propeptides and cleaved forms of caspase-3 and PARP ( a ). Density analysis of the activation of caspase-3 ( b ) and PARP ( c ), shown as the ratios of cleavage to propeptide content, followed by normalization to negative control (NC) levels. IHC staining for active PARP peptides ( d ) and labeling index ( e ) quantitatively demonstrated that PD90780 administration potentiated the increase of PARP activation in BDL-treated mouse livers. ( f ) Representative microphotographs of TUNEL staining showing the apoptotic events in mouse liver sections. Scale bars=50 μm. ( g ) Analysis of TUNEL-positive parenchymal cells indicated that recombinant NGF administration exerted a protective effect, whereas treatment with a p75NTR antagonist, PD90780, increased apoptotic cell death in BDL-induced cholestatic injured livers. All data are shown as the mean±s.e.m. * P <0.05 between indicated groups. ND, not detectable. NS, not significant.

    Article Snippet: A p75NTR blocker, PD90780, was purchased from Axon Medchem (Groningen, The Netherlands).

    Techniques: Ligation, Recombinant, Western Blot, Activation Assay, Negative Control, Immunohistochemistry, Labeling, TUNEL Assay, Staining

    Effects of simultaneous administration with NGF and its receptor blockers on bile duct ligation (BDL)-induced mouse liver injury. The ICR mice receiving BDL surgery were intraperitoneally administered recombinant NGF (1 mg kg −1 ; n =3) twice weekly and simultaneous daily injections of PBS ( n =6), GW441756 (GW; 1 mg kg −1 ; n =6), DMSO ( n =6) or PD90780 (PD; 1 mg kg −1 ; n =6). At 14 days postoperation, serum levels of AST ( a ) and total bilirubin ( b ) were biochemically measured, whereas serum interleukin (IL)-6 levels ( c ) were analyzed by ELISA. ( d ) The representative H&E staining results showing the necrotic regions in cholestasis-injured livers. Scale bar=1000 μm. ( e ) Morphometric analysis of necrotic region areas. All data are shown as the mean±s.e.m. * P <0.05 between the indicated groups. ND, not detectable. NS, not significant.

    Journal: Experimental & Molecular Medicine

    Article Title: Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

    doi: 10.1038/emm.2017.235

    Figure Lengend Snippet: Effects of simultaneous administration with NGF and its receptor blockers on bile duct ligation (BDL)-induced mouse liver injury. The ICR mice receiving BDL surgery were intraperitoneally administered recombinant NGF (1 mg kg −1 ; n =3) twice weekly and simultaneous daily injections of PBS ( n =6), GW441756 (GW; 1 mg kg −1 ; n =6), DMSO ( n =6) or PD90780 (PD; 1 mg kg −1 ; n =6). At 14 days postoperation, serum levels of AST ( a ) and total bilirubin ( b ) were biochemically measured, whereas serum interleukin (IL)-6 levels ( c ) were analyzed by ELISA. ( d ) The representative H&E staining results showing the necrotic regions in cholestasis-injured livers. Scale bar=1000 μm. ( e ) Morphometric analysis of necrotic region areas. All data are shown as the mean±s.e.m. * P <0.05 between the indicated groups. ND, not detectable. NS, not significant.

    Article Snippet: A p75NTR blocker, PD90780, was purchased from Axon Medchem (Groningen, The Netherlands).

    Techniques: Ligation, Recombinant, Enzyme-linked Immunosorbent Assay, Staining

    Effects of simultaneous administration with NGF and its receptor blockers on bile duct ligation (BDL)-induced apoptosis of parenchymal hepatocytes. The ICR mice receiving BDL surgery were intraperitoneally administered recombinant NGF (1 mg kg −1 ; n =3) twice weekly and simultaneous daily injections of PBS ( n =6), GW441756 (GW; 1 mg kg −1 ; n =6), DMSO ( n =6) or PD90780 (PD; 1 mg kg −1 ; n =6). After 2 weeks of treatment, pooled liver extracts of each group were subjected to western blotting to detect both propeptides and cleaved forms of caspase-3 and PARP ( a ). The activation of caspase-3 ( b ) and PARP ( c ) was densitometrically analyzed and is shown as the cleavage-to-propeptide ratios and normalized to negative control (NC) levels. ( d ) Representative images of IHC staining for activated PARP in the mouse livers. ( e ) Quantitative measurement of PARP activation as shown by labeling index. ( f ) Representative microphotographs of TUNEL staining showing the apoptotic events in mouse liver sections. Scale bars=50 μm. ( g ) Analysis of TUNEL-positive parenchymal cells indicated that GW treatment significantly increased apoptotic cell death in BDL-induced cholestatic injured livers. All data are shown as the mean±s.e.m. * P <0.05 between indicated groups. ND, not detectable. NS, not significant.

    Journal: Experimental & Molecular Medicine

    Article Title: Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

    doi: 10.1038/emm.2017.235

    Figure Lengend Snippet: Effects of simultaneous administration with NGF and its receptor blockers on bile duct ligation (BDL)-induced apoptosis of parenchymal hepatocytes. The ICR mice receiving BDL surgery were intraperitoneally administered recombinant NGF (1 mg kg −1 ; n =3) twice weekly and simultaneous daily injections of PBS ( n =6), GW441756 (GW; 1 mg kg −1 ; n =6), DMSO ( n =6) or PD90780 (PD; 1 mg kg −1 ; n =6). After 2 weeks of treatment, pooled liver extracts of each group were subjected to western blotting to detect both propeptides and cleaved forms of caspase-3 and PARP ( a ). The activation of caspase-3 ( b ) and PARP ( c ) was densitometrically analyzed and is shown as the cleavage-to-propeptide ratios and normalized to negative control (NC) levels. ( d ) Representative images of IHC staining for activated PARP in the mouse livers. ( e ) Quantitative measurement of PARP activation as shown by labeling index. ( f ) Representative microphotographs of TUNEL staining showing the apoptotic events in mouse liver sections. Scale bars=50 μm. ( g ) Analysis of TUNEL-positive parenchymal cells indicated that GW treatment significantly increased apoptotic cell death in BDL-induced cholestatic injured livers. All data are shown as the mean±s.e.m. * P <0.05 between indicated groups. ND, not detectable. NS, not significant.

    Article Snippet: A p75NTR blocker, PD90780, was purchased from Axon Medchem (Groningen, The Netherlands).

    Techniques: Ligation, Recombinant, Western Blot, Activation Assay, Negative Control, Immunohistochemistry, Labeling, TUNEL Assay, Staining

    Involvement of NGF-induced SIRT1 upregulation in hepatocytes under oxidative stress. ( a ) Huh-7 hepatocytes were treated with either NGF or proNGF for 24 h. Western blotting detection indicated that NGF, but not proNGF, upregulated SIRT1 expression in human hepatocytes. ( b ) SIRT1 upregulation by NGF stimulation in cultured rat and mouse primary hepatocytes. ( c ) Kinetic profiles of NGF-mediated signaling activation. Huh-7 cells were treated with NGF for the indicated durations and measured by western blotting. ( d ) Involvement of NF-κB and SIRT1 activities in the NGF-induced SIRT1 upregulation. Huh-7 cells were pretreated with 10 μ M PDTC or 20 μM EX-527 for 2 h, followed by 2 or 24 h of NGF stimulation. ( e ) Effects of NGFR blockers, kinase inhibitors and SIRT1 modulators on oxidative stress-activated pro-apoptotic machinery. Huh-7 cells were pretreated either with 20 μ M resveratrol (RSV; a SIRT1 agonist) or with 10 ng ml −1 NGF for 24 h in the presence of 10 μ M NGFR blockers (GW441756 and PD90780), 10 μ M kinase blockers (PDTC, LY294002 and PD98059), 20 μ M EX-527 (a SIRT1 antagonist) or equivalent DMSO, followed by 1-h transient exposure to 0.8 m M H 2 O 2 . After H 2 O 2 removal and another 4-h incubation, protein lysates were collected for western blotting detection of caspase-3 and PARP. The density analysis data are shown in . ( f ) Effects of NGFR blockers, kinase inhibitors and SIRT1 modulators on oxidative stress-induced hepatotoxicity as measured by MTT-based cell viability assay. All data are shown as the mean±s.d. of three independent experiments. * P <0.05 vs DMSO solvent control or between the indicated groups; # P <0.05 vs the H 2 O 2 treatment group.

    Journal: Experimental & Molecular Medicine

    Article Title: Nerve growth factor upregulates sirtuin 1 expression in cholestasis: a potential therapeutic target

    doi: 10.1038/emm.2017.235

    Figure Lengend Snippet: Involvement of NGF-induced SIRT1 upregulation in hepatocytes under oxidative stress. ( a ) Huh-7 hepatocytes were treated with either NGF or proNGF for 24 h. Western blotting detection indicated that NGF, but not proNGF, upregulated SIRT1 expression in human hepatocytes. ( b ) SIRT1 upregulation by NGF stimulation in cultured rat and mouse primary hepatocytes. ( c ) Kinetic profiles of NGF-mediated signaling activation. Huh-7 cells were treated with NGF for the indicated durations and measured by western blotting. ( d ) Involvement of NF-κB and SIRT1 activities in the NGF-induced SIRT1 upregulation. Huh-7 cells were pretreated with 10 μ M PDTC or 20 μM EX-527 for 2 h, followed by 2 or 24 h of NGF stimulation. ( e ) Effects of NGFR blockers, kinase inhibitors and SIRT1 modulators on oxidative stress-activated pro-apoptotic machinery. Huh-7 cells were pretreated either with 20 μ M resveratrol (RSV; a SIRT1 agonist) or with 10 ng ml −1 NGF for 24 h in the presence of 10 μ M NGFR blockers (GW441756 and PD90780), 10 μ M kinase blockers (PDTC, LY294002 and PD98059), 20 μ M EX-527 (a SIRT1 antagonist) or equivalent DMSO, followed by 1-h transient exposure to 0.8 m M H 2 O 2 . After H 2 O 2 removal and another 4-h incubation, protein lysates were collected for western blotting detection of caspase-3 and PARP. The density analysis data are shown in . ( f ) Effects of NGFR blockers, kinase inhibitors and SIRT1 modulators on oxidative stress-induced hepatotoxicity as measured by MTT-based cell viability assay. All data are shown as the mean±s.d. of three independent experiments. * P <0.05 vs DMSO solvent control or between the indicated groups; # P <0.05 vs the H 2 O 2 treatment group.

    Article Snippet: A p75NTR blocker, PD90780, was purchased from Axon Medchem (Groningen, The Netherlands).

    Techniques: Western Blot, Expressing, Cell Culture, Activation Assay, Incubation, Viability Assay, Solvent, Control

    Table 2.

    Journal:

    Article Title: Role of p75 NTR in female rat urinary bladder with cyclophosphamide-induced cystitis

    doi: 10.1152/ajprenal.90501.2008

    Figure Lengend Snippet: Table 2.

    Article Snippet: PD90780 was obtained through a compound transfer agreement with Pfizer (Groton, CT).

    Techniques: