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polyclonal rabbit anti gdnf antibody  (Bioss)


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    Bioss polyclonal rabbit anti gdnf antibody
    Polyclonal Rabbit Anti Gdnf Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 6 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 6 article reviews
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    94/100 stars

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    The effects of <t>GDNF</t> overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)
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    The effects of <t>GDNF</t> overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)
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    The effects of <t>GDNF</t> overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)
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    Bioss polyclonal rabbit antigdnf antibody
    The effects of <t>GDNF</t> overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)
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    Histological images of hippocampus (A–E) and pyknotic index in the dentate gyrus of the hippocampus in male rats under stress exposures (F). The black arrow indicates a normal granular cell, characterized by a dark-staining nucleus and scanty cytoplasm. The black asterisk indicates pyknotic nuclei, small condensed, dark-staining nuclei with eosinophilic cytoplasm. Relative glial cell-derived neurotrophic factor <t>(GDNF)</t> protein in hippocampus in stressed rats (G) and the representative expression of GDNF to GAPDH (H). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.
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    Histological images of hippocampus (A–E) and pyknotic index in the dentate gyrus of the hippocampus in male rats under stress exposures (F). The black arrow indicates a normal granular cell, characterized by a dark-staining nucleus and scanty cytoplasm. The black asterisk indicates pyknotic nuclei, small condensed, dark-staining nuclei with eosinophilic cytoplasm. Relative glial cell-derived neurotrophic factor <t>(GDNF)</t> protein in hippocampus in stressed rats (G) and the representative expression of GDNF to GAPDH (H). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.
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    Santa Cruz Biotechnology rabbit anti-gdnf polyclonal antibody
    Chronic morphine reduced the level of <t>GDNF</t> in the spinal cord of BCP rats. ( A , B ) The immunochemistry test demonstrated that GDNF was located in the superficial laminae of the spinal cord. Compared with the sham operated rats treated with normal saline (sham+NS), the expression of GDNF was reduced in the BCP rats treated with normal saline (BCP+NS) and morphine (BCP+MT). n = 3 rats. *** p < 0.001, significantly different from sham +NS group. # p < 0.05, significantly different from the BCP+NS group. Scale bar = 200 μm. ( C ) Western blot demonstrated that expression of GDNF was decreased in BCP+MT rats compared with both the sham+NS and BCP+NS rats. n = 4 rats. *** p < 0.001, significantly different from the sham+NS group. # p < 0.05, significantly different from the BCP+NS group. ( D ) Western blot demonstrated that expression of GDNF was time-dependently reduced after chronic morphine treatment. n = 4 rats. ** p < 0.01, significantly different from the expression on Day 1.
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    Image Search Results


    The effects of GDNF overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: The effects of GDNF overexpression in astrocytes on synaptic proteins following PT. (a) An illustration of the viral injection. IC: ischemic core; PIR: peri-infarct region. (b) Experimental timeline. (c , d) Fluorescent images showing the expressions of GDNF and mRFP in cortical astrocytes 7 days after PT. (e-l) WB images (e) and summary data (f-l) of protein expressions in cortical tissues 7 days after PT. In (c-l) rAAV5-GDNF and rAAV5-mRFP virus were injected 2 weeks before PT. N = 4 mice for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Over Expression, Injection, Virus

    Overexpression of GDNF in astrocytes reduced brain lesion and promoted motor function recovery after PT. (a) Representative images of Nissl staining showing the brain infarct areas of viral injected mice 2 days after PT. The white dash lines outline the damage area. (b , c) Quantification of infarct volumes at 2 (b) and 7 (c) days after PT. N = 4 mice for each group 2 days after PT and 7 mice for each group 7 days after PT. (d-g) Evaluation of motor behavior function by cylinder (d , e) , hanging wire (f) , and grip force (g) tests at different timepoints before and after PT. N = 8 and 7 mice injected with rAAV5-mRFP and rAAV5-GDNF vectors. * p < 0.05, ** p < 0.01, ***<0.001; (Student’s t-test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Overexpression of GDNF in astrocytes reduced brain lesion and promoted motor function recovery after PT. (a) Representative images of Nissl staining showing the brain infarct areas of viral injected mice 2 days after PT. The white dash lines outline the damage area. (b , c) Quantification of infarct volumes at 2 (b) and 7 (c) days after PT. N = 4 mice for each group 2 days after PT and 7 mice for each group 7 days after PT. (d-g) Evaluation of motor behavior function by cylinder (d , e) , hanging wire (f) , and grip force (g) tests at different timepoints before and after PT. N = 8 and 7 mice injected with rAAV5-mRFP and rAAV5-GDNF vectors. * p < 0.05, ** p < 0.01, ***<0.001; (Student’s t-test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Over Expression, Staining, Injection

    GDNF overexpression promoted proliferation of reactive astrocytes and reduced oxidative stress in PIR following PI. (a-d) Representative fluorescent images and signal analysis of GFAP (a , b) and Iba 1 (c , d) expressions in the PIR from rAAV5-mRFP and rAAV5-GDNF viruses injected mice at day 4 post stroke. The right panels were the high-resolution images of the boxed region in the left panels. N = 4 mice for each group. (e-f) Fluorescent images of DHE and Dapi and analysis of DHE signal in the PIR of mRFP and GDNF viruses transduced mice at 4 days after stroke. The right panels were the high-resolution images of the boxed region in the left panels. Notice the decreases in DHE signal in GDNF overexpression mice. Data were averaged from 10 images for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: GDNF overexpression promoted proliferation of reactive astrocytes and reduced oxidative stress in PIR following PI. (a-d) Representative fluorescent images and signal analysis of GFAP (a , b) and Iba 1 (c , d) expressions in the PIR from rAAV5-mRFP and rAAV5-GDNF viruses injected mice at day 4 post stroke. The right panels were the high-resolution images of the boxed region in the left panels. N = 4 mice for each group. (e-f) Fluorescent images of DHE and Dapi and analysis of DHE signal in the PIR of mRFP and GDNF viruses transduced mice at 4 days after stroke. The right panels were the high-resolution images of the boxed region in the left panels. Notice the decreases in DHE signal in GDNF overexpression mice. Data were averaged from 10 images for each group. * p < 0.05, ** p < 0.01, *** p < 0.001; (Student’s t-test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Over Expression, Injection

    Astrocyte-derived GDNF reduced neuronal death after OGD. (a , b) WB images and analysis of GDNF expression in primary cultured astrocytes (a) and GDNF content in the medium (b) at different conditions. N = 4 independent experiments. For OGD condition, primary cultured astrocytes were subjected to 6 h OGD and followed by 24 h reperfusion for western blot and ELISA analysis. (c) Schematic diagram showing experimental design. Primary astrocytes with or without transfection of GDNF plasmid were subjected to 6 h OGD. Astrocyte conditioned medium from astrocyte cultures not subjected or subjected to OGD, namely ACM and ACM(OGD) of different conditions were collected 24 h later and added to primary neuronal cultures after subjected to 1 h OGD followed by 24 h reoxygenation for neuronal viability and death assays. (d-f) Neuronal viability, percentages of PI + neurons and neurons with condensed nuclei after 1 h OGD and followed by 24 h reoxygenation at different conditions. The percentage of PI + neurons was calculated based on the total number of neurons based on DAPI staining. (g) Fluorescent images of neurons stained with PI and Dapi at different conditions. Data in (d) were averaged values from 6 replicates of representative experiment; data in (e , f) were averaged from cell counting of 9 images in each condition. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Astrocyte-derived GDNF reduced neuronal death after OGD. (a , b) WB images and analysis of GDNF expression in primary cultured astrocytes (a) and GDNF content in the medium (b) at different conditions. N = 4 independent experiments. For OGD condition, primary cultured astrocytes were subjected to 6 h OGD and followed by 24 h reperfusion for western blot and ELISA analysis. (c) Schematic diagram showing experimental design. Primary astrocytes with or without transfection of GDNF plasmid were subjected to 6 h OGD. Astrocyte conditioned medium from astrocyte cultures not subjected or subjected to OGD, namely ACM and ACM(OGD) of different conditions were collected 24 h later and added to primary neuronal cultures after subjected to 1 h OGD followed by 24 h reoxygenation for neuronal viability and death assays. (d-f) Neuronal viability, percentages of PI + neurons and neurons with condensed nuclei after 1 h OGD and followed by 24 h reoxygenation at different conditions. The percentage of PI + neurons was calculated based on the total number of neurons based on DAPI staining. (g) Fluorescent images of neurons stained with PI and Dapi at different conditions. Data in (d) were averaged values from 6 replicates of representative experiment; data in (e , f) were averaged from cell counting of 9 images in each condition. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Derivative Assay, Expressing, Cell Culture, Western Blot, Enzyme-linked Immunosorbent Assay, Transfection, Plasmid Preparation, Staining, Cell Counting

    Reactive astrocytes-derived GDNF triggered the activation of RET receptors in primary neurons after OGD. (a-e) WB images of protein expressions (a) and analysis (b-e) in primary cultured neurons after OGD. Summary data in (b-e) were averaged from 4 replicates. * p < 0.05, ** p < 0.01; (one-way ANOVA test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Reactive astrocytes-derived GDNF triggered the activation of RET receptors in primary neurons after OGD. (a-e) WB images of protein expressions (a) and analysis (b-e) in primary cultured neurons after OGD. Summary data in (b-e) were averaged from 4 replicates. * p < 0.05, ** p < 0.01; (one-way ANOVA test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Derivative Assay, Activation Assay, Cell Culture

    Astrocyte-derived GDNF protected neurons against OGD through the activation of neuronal GDNF receptors. (a-c) Neuronal viability and death based on PI staining and condensed nuclei after 1 h OGD and followed by 24 h reoxygenation at different conditions. (d) Representative fluorescent images of neurons stained with PI and Dapi at different conditions. Data in (a) were averaged values for 6 replicates of representative experiment; data in (b , c) were averaged from cell counting in 9 images in each condition. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Astrocyte-derived GDNF protected neurons against OGD through the activation of neuronal GDNF receptors. (a-c) Neuronal viability and death based on PI staining and condensed nuclei after 1 h OGD and followed by 24 h reoxygenation at different conditions. (d) Representative fluorescent images of neurons stained with PI and Dapi at different conditions. Data in (a) were averaged values for 6 replicates of representative experiment; data in (b , c) were averaged from cell counting in 9 images in each condition. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Derivative Assay, Activation Assay, Staining, Cell Counting

    Reactive astrocyte-derived GDNF inhibited mitochondrial fission and apoptosis of primary neurons after OGD. (a-g) WB images (a) and analysis (b-g) of protein expressions in primary neurons after OGD. Data were from 3–4 independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Reactive astrocyte-derived GDNF inhibited mitochondrial fission and apoptosis of primary neurons after OGD. (a-g) WB images (a) and analysis (b-g) of protein expressions in primary neurons after OGD. Data were from 3–4 independent experiments. * p < 0.05, ** p < 0.01, *** p < 0.001; (one-way ANOVA test)

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Derivative Assay

    Schematic diagram illustrating the role of astrocytic GDNF in neuronal survival and brain recovery after ischemic stroke. Astrocytes are activated following ischemic stroke and become reactive astrocytes. Reactive astrocytes release GDNF into extracellular space and binds to GFRα1 protein anchor on neuronal cell membrane. The GDNF-GFRα1 complexes trigger the phosphorylation of RET receptors in neurons and initiate intracellular signaling pathways, which suppress mitochondrial fission and reduce oxidative stress. These changes inhibit caspase regulated cell apoptosis and promote neuronal survival and brain recovery after ischemic stroke

    Journal: Neurochemical Research

    Article Title: Reactive Astrocytes Release GDNF to Promote Brain Recovery and Neuronal Survival Following Ischemic Stroke

    doi: 10.1007/s11064-025-04370-6

    Figure Lengend Snippet: Schematic diagram illustrating the role of astrocytic GDNF in neuronal survival and brain recovery after ischemic stroke. Astrocytes are activated following ischemic stroke and become reactive astrocytes. Reactive astrocytes release GDNF into extracellular space and binds to GFRα1 protein anchor on neuronal cell membrane. The GDNF-GFRα1 complexes trigger the phosphorylation of RET receptors in neurons and initiate intracellular signaling pathways, which suppress mitochondrial fission and reduce oxidative stress. These changes inhibit caspase regulated cell apoptosis and promote neuronal survival and brain recovery after ischemic stroke

    Article Snippet: The primary antibodies include a mouse anti-GFAP monoclonal antibody (1:300; Cat. No. MAB360, Sigma), a rabbit anti-GDNF polyclonal antibody (1:300, Cat. No. SC-328, Santa Cruz Biotechnology), a rabbit anti-Iba 1 polyclonal antibody (1:300, Cat. No. 019-19741, Fujifilm).

    Techniques: Membrane, Phospho-proteomics, Protein-Protein interactions

    Histological images of hippocampus (A–E) and pyknotic index in the dentate gyrus of the hippocampus in male rats under stress exposures (F). The black arrow indicates a normal granular cell, characterized by a dark-staining nucleus and scanty cytoplasm. The black asterisk indicates pyknotic nuclei, small condensed, dark-staining nuclei with eosinophilic cytoplasm. Relative glial cell-derived neurotrophic factor (GDNF) protein in hippocampus in stressed rats (G) and the representative expression of GDNF to GAPDH (H). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.

    Journal: PeerJ

    Article Title: Stress-induced changes in cognitive function and intestinal barrier integrity can be ameliorated by venlafaxine and synbiotic supplementations

    doi: 10.7717/peerj.17033

    Figure Lengend Snippet: Histological images of hippocampus (A–E) and pyknotic index in the dentate gyrus of the hippocampus in male rats under stress exposures (F). The black arrow indicates a normal granular cell, characterized by a dark-staining nucleus and scanty cytoplasm. The black asterisk indicates pyknotic nuclei, small condensed, dark-staining nuclei with eosinophilic cytoplasm. Relative glial cell-derived neurotrophic factor (GDNF) protein in hippocampus in stressed rats (G) and the representative expression of GDNF to GAPDH (H). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.

    Article Snippet: These membranes were then subjected to overnight incubation at 4 °C with either a 1:1,000 dilution of rabbit polyclonal anti-GDNF antibody (catalog no. Cat #PA5-89957; Invitrogen, Thermo Fisher Scientific, Waltham, MA, USA), a 1:5,000 dilution of rabbit polyclonal anti-β-actin antibody (catalog no. AB8227; Abcam, Cambridge, UK) or GAPDH antibody (catalog no. Cat #PA1-988; Invitrogen, Thermo Fisher Scientific, Waltham, MA, USA).

    Techniques: Staining, Derivative Assay, Expressing, Control

    Histological images of ileum (A–E) and inflammatory scores in male rats under stress exposures (F). The morphology of the ileum revealed desquamation of the villi (black star), villous edema (black triangle), loss of villi (asterisks) and layer separation (black arrow). 70-kDa FITC-dextran intestinal permeability (G), relative glial cell-derived neurotrophic factor (GDNF) protein in ileum in stressed rats (H) and the representative expression of GDNF beta actin (I). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 and ††† p < 0.001 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.

    Journal: PeerJ

    Article Title: Stress-induced changes in cognitive function and intestinal barrier integrity can be ameliorated by venlafaxine and synbiotic supplementations

    doi: 10.7717/peerj.17033

    Figure Lengend Snippet: Histological images of ileum (A–E) and inflammatory scores in male rats under stress exposures (F). The morphology of the ileum revealed desquamation of the villi (black star), villous edema (black triangle), loss of villi (asterisks) and layer separation (black arrow). 70-kDa FITC-dextran intestinal permeability (G), relative glial cell-derived neurotrophic factor (GDNF) protein in ileum in stressed rats (H) and the representative expression of GDNF beta actin (I). * p < 0.05, ** p < 0.01 and *** p < 0.001 compared to vehicle-treated control rats. † p < 0.05 and ††† p < 0.001 compared to vehicle-treated stressed rats ( n = 4 rats/group). Con, control; Str, stressed+vehicle; Str+Vlx, stressed+venlafaxine; Str+Syn, stressed+synbiotic supplement; Str+Vlx+Syn, stressed+venlafaxine+synbiotic supplement.

    Article Snippet: These membranes were then subjected to overnight incubation at 4 °C with either a 1:1,000 dilution of rabbit polyclonal anti-GDNF antibody (catalog no. Cat #PA5-89957; Invitrogen, Thermo Fisher Scientific, Waltham, MA, USA), a 1:5,000 dilution of rabbit polyclonal anti-β-actin antibody (catalog no. AB8227; Abcam, Cambridge, UK) or GAPDH antibody (catalog no. Cat #PA1-988; Invitrogen, Thermo Fisher Scientific, Waltham, MA, USA).

    Techniques: Permeability, Derivative Assay, Expressing, Control

    Chronic morphine reduced the level of GDNF in the spinal cord of BCP rats. ( A , B ) The immunochemistry test demonstrated that GDNF was located in the superficial laminae of the spinal cord. Compared with the sham operated rats treated with normal saline (sham+NS), the expression of GDNF was reduced in the BCP rats treated with normal saline (BCP+NS) and morphine (BCP+MT). n = 3 rats. *** p < 0.001, significantly different from sham +NS group. # p < 0.05, significantly different from the BCP+NS group. Scale bar = 200 μm. ( C ) Western blot demonstrated that expression of GDNF was decreased in BCP+MT rats compared with both the sham+NS and BCP+NS rats. n = 4 rats. *** p < 0.001, significantly different from the sham+NS group. # p < 0.05, significantly different from the BCP+NS group. ( D ) Western blot demonstrated that expression of GDNF was time-dependently reduced after chronic morphine treatment. n = 4 rats. ** p < 0.01, significantly different from the expression on Day 1.

    Journal: Brain Sciences

    Article Title: Overexpression of GDNF in Spinal Cord Attenuates Morphine Analgesic Tolerance in Rats with Bone Cancer Pain

    doi: 10.3390/brainsci12091188

    Figure Lengend Snippet: Chronic morphine reduced the level of GDNF in the spinal cord of BCP rats. ( A , B ) The immunochemistry test demonstrated that GDNF was located in the superficial laminae of the spinal cord. Compared with the sham operated rats treated with normal saline (sham+NS), the expression of GDNF was reduced in the BCP rats treated with normal saline (BCP+NS) and morphine (BCP+MT). n = 3 rats. *** p < 0.001, significantly different from sham +NS group. # p < 0.05, significantly different from the BCP+NS group. Scale bar = 200 μm. ( C ) Western blot demonstrated that expression of GDNF was decreased in BCP+MT rats compared with both the sham+NS and BCP+NS rats. n = 4 rats. *** p < 0.001, significantly different from the sham+NS group. # p < 0.05, significantly different from the BCP+NS group. ( D ) Western blot demonstrated that expression of GDNF was time-dependently reduced after chronic morphine treatment. n = 4 rats. ** p < 0.01, significantly different from the expression on Day 1.

    Article Snippet: The sections of spinal cord were blocked with 10% normal donkey serum and 0.1% Triton X-100 in PBS for 1 h at 24 °C and then treated with rabbit anti-GDNF polyclonal antibody (1:100, Santa Cruz), mouse anti-MOR antibody (1:100, Abcam), and incubated at 4 °C in the refrigerator overnight.

    Techniques: Saline, Expressing, Western Blot

    LV-GDNF intrathecal injection upregulated GDNF in the spinal cord of MT rats with BCP. ( A ) GFP expression was detected in the spinal cord of bone cancer pain and morphine tolerance rats treated with lentivirus-mediated GDNF (BM+LV-GDNF) and lentivirus of negative control (BM+LV-NC), but not in the BM rats treated with normal saline (BM+NS). Scale bar = 200 μm. ( B,C ) The overexpression of GDNF was detected by the immunochemistry test and Western blot in the spinal cord of the BM+LV-GDNF rats. n = 4 rats. *** p < 0.001, significantly different from the BM+LV-GDNF group.

    Journal: Brain Sciences

    Article Title: Overexpression of GDNF in Spinal Cord Attenuates Morphine Analgesic Tolerance in Rats with Bone Cancer Pain

    doi: 10.3390/brainsci12091188

    Figure Lengend Snippet: LV-GDNF intrathecal injection upregulated GDNF in the spinal cord of MT rats with BCP. ( A ) GFP expression was detected in the spinal cord of bone cancer pain and morphine tolerance rats treated with lentivirus-mediated GDNF (BM+LV-GDNF) and lentivirus of negative control (BM+LV-NC), but not in the BM rats treated with normal saline (BM+NS). Scale bar = 200 μm. ( B,C ) The overexpression of GDNF was detected by the immunochemistry test and Western blot in the spinal cord of the BM+LV-GDNF rats. n = 4 rats. *** p < 0.001, significantly different from the BM+LV-GDNF group.

    Article Snippet: The sections of spinal cord were blocked with 10% normal donkey serum and 0.1% Triton X-100 in PBS for 1 h at 24 °C and then treated with rabbit anti-GDNF polyclonal antibody (1:100, Santa Cruz), mouse anti-MOR antibody (1:100, Abcam), and incubated at 4 °C in the refrigerator overnight.

    Techniques: Injection, Expressing, Negative Control, Saline, Over Expression, Western Blot

    Upregulation of GDNF alleviated morphine tolerance in bone cancer pain rats. The mechanical ( A ) and thermal ( B ) withdrawal threshold indicated that LV-GDNF injection alleviated the morphine analgesic tolerance in BCP rats. n = 8 rats. * p < 0.05, ** p < 0.01, *** p < 0.001, significantly different from bone cancer pain and morphine tolerance rats treated with normal saline (BM+NS). ( C ) The percentage of the maximum possible effect (%MPE) of morphine was detected by the tail-flick latency test in the bone cancer pain rats. n = 8 rats. ** p < 0.01, *** p < 0.001, significantly different from BM rats treated with normal saline (BM+NS). ( D ) Time course of morphine analgesic effect in BM rats was detected by the thermal paw withdrawal latency on POD 15. n = 8 rats. ** p < 0.01, *** p < 0.001, significantly different from BM+NS group. ###, p < 0.001, compared with the corresponding baseline.

    Journal: Brain Sciences

    Article Title: Overexpression of GDNF in Spinal Cord Attenuates Morphine Analgesic Tolerance in Rats with Bone Cancer Pain

    doi: 10.3390/brainsci12091188

    Figure Lengend Snippet: Upregulation of GDNF alleviated morphine tolerance in bone cancer pain rats. The mechanical ( A ) and thermal ( B ) withdrawal threshold indicated that LV-GDNF injection alleviated the morphine analgesic tolerance in BCP rats. n = 8 rats. * p < 0.05, ** p < 0.01, *** p < 0.001, significantly different from bone cancer pain and morphine tolerance rats treated with normal saline (BM+NS). ( C ) The percentage of the maximum possible effect (%MPE) of morphine was detected by the tail-flick latency test in the bone cancer pain rats. n = 8 rats. ** p < 0.01, *** p < 0.001, significantly different from BM rats treated with normal saline (BM+NS). ( D ) Time course of morphine analgesic effect in BM rats was detected by the thermal paw withdrawal latency on POD 15. n = 8 rats. ** p < 0.01, *** p < 0.001, significantly different from BM+NS group. ###, p < 0.001, compared with the corresponding baseline.

    Article Snippet: The sections of spinal cord were blocked with 10% normal donkey serum and 0.1% Triton X-100 in PBS for 1 h at 24 °C and then treated with rabbit anti-GDNF polyclonal antibody (1:100, Santa Cruz), mouse anti-MOR antibody (1:100, Abcam), and incubated at 4 °C in the refrigerator overnight.

    Techniques: Injection, Saline, Tail Flick Test

    Upregulation of GDNF recovered MOR expression in morphine tolerance rats with bone cancer pain. ( A ) MOR expression was reduced in the spinal cord of bone cancer pain rats treated with normal saline (BCP+NS), and further downregulated in BCP rats with morphine tolerance (BCP+MT). Scale bar = 200 μm. ( B ) The double immunochemistry test demonstrated that GDNF and MOR were coexpressed in the spinal cord of rats. Scale bar = 200 μm. ( C , D ) The expression of MOR in the spinal cord of morphine tolerance rats with bone cancer pain was restored by LV-GDNF injection, but not LV-NC intrathecal injection. n = 4 rats. ** p < 0.01, significantly different from the LV-NC group.

    Journal: Brain Sciences

    Article Title: Overexpression of GDNF in Spinal Cord Attenuates Morphine Analgesic Tolerance in Rats with Bone Cancer Pain

    doi: 10.3390/brainsci12091188

    Figure Lengend Snippet: Upregulation of GDNF recovered MOR expression in morphine tolerance rats with bone cancer pain. ( A ) MOR expression was reduced in the spinal cord of bone cancer pain rats treated with normal saline (BCP+NS), and further downregulated in BCP rats with morphine tolerance (BCP+MT). Scale bar = 200 μm. ( B ) The double immunochemistry test demonstrated that GDNF and MOR were coexpressed in the spinal cord of rats. Scale bar = 200 μm. ( C , D ) The expression of MOR in the spinal cord of morphine tolerance rats with bone cancer pain was restored by LV-GDNF injection, but not LV-NC intrathecal injection. n = 4 rats. ** p < 0.01, significantly different from the LV-NC group.

    Article Snippet: The sections of spinal cord were blocked with 10% normal donkey serum and 0.1% Triton X-100 in PBS for 1 h at 24 °C and then treated with rabbit anti-GDNF polyclonal antibody (1:100, Santa Cruz), mouse anti-MOR antibody (1:100, Abcam), and incubated at 4 °C in the refrigerator overnight.

    Techniques: Expressing, Saline, Injection