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gdnf polyclonal antibody (Proteintech)

Name: gdnf polyclonal antibody
Brand: Proteintech
Rating: 93 (11 reviews)

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Proteintech gdnf polyclonal antibody

Muse cell has protective effects on DA neurons. A : (200×magnification) Compared to normal WT mice, the PBS group showed reduced TH and NeuN staining in the SNc region. In contrast to the PBS group, the muse group exhibited a higher number of TH-positive cells and NeuN-positive cells, with PKH26-labeled muse cells present in the region. Compared to the muse group, the muse + J and non-muse groups displayed relatively fewer TH-positive cells( n = 6). B : S1P expression in the brain tissue of A53T mice (PBS group) was significantly increased compared with normal WT mice. In the group treated with muse cells, S1P expression was markedly reduced relative to both the PBS and non-muse groups, though it remained higher than that in normal WT mice. Western blot results indicated: TNF-α expression in the brains of the PBS group was significantly higher than in control. Compared to the PBS group, TNF-α expression was significantly reduced in the muse group, while the non-muse and muse + J groups also showed reduced TNF-α expression. TNF-α expression in the muse group was lower than in the non-muse and muse + J groups. Expression levels of BDNF and <t>GDNF</t> showed a marked decline in the PBS group. No significant change was seen with non-muse cell treatment, whereas the muse group displayed elevated expression. The expression remained unchanged in the muse + J group. (*Compared to the control group, ** P < 0.01, and compared to the PBS group, # P < 0.05, ## P < 0.01, & compared to the muse group, & P < 0.05) ( n = 3). C : The H&E staining results (200× magnification) showed that in the substantia nigra region of normal WT mice, the tissue structure was normal, and the cell nuclei were clearly visible (red arrows indicate astrocytes, green arrows indicate neuronal cells). In contrast, the brains of PBS group mice exhibited significant neuronal loss, with abnormal neuronal nuclear morphology and blurred boundaries. The non-muse group and muse + J group showed similar conditions to the PBS group, but the degree of neuronal damage was reduced. In the muse group, the number of damaged neurons was significantly decreased, and the tissue characteristics were similar to those of normal WT mice. (red→astrocyte, green→neuronal cells, black→damaged neuronal cells) ( n = 6)

Gdnf Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 11 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Intranasally administered muse cells attenuate neurodegeneration in Parkinson’s disease"

Article Title: Intranasally administered muse cells attenuate neurodegeneration in Parkinson’s disease

Journal: Journal of Translational Medicine

doi: 10.1186/s12967-025-07401-6

Figure Legend Snippet: Muse cell has protective effects on DA neurons. A : (200×magnification) Compared to normal WT mice, the PBS group showed reduced TH and NeuN staining in the SNc region. In contrast to the PBS group, the muse group exhibited a higher number of TH-positive cells and NeuN-positive cells, with PKH26-labeled muse cells present in the region. Compared to the muse group, the muse + J and non-muse groups displayed relatively fewer TH-positive cells( n = 6). B : S1P expression in the brain tissue of A53T mice (PBS group) was significantly increased compared with normal WT mice. In the group treated with muse cells, S1P expression was markedly reduced relative to both the PBS and non-muse groups, though it remained higher than that in normal WT mice. Western blot results indicated: TNF-α expression in the brains of the PBS group was significantly higher than in control. Compared to the PBS group, TNF-α expression was significantly reduced in the muse group, while the non-muse and muse + J groups also showed reduced TNF-α expression. TNF-α expression in the muse group was lower than in the non-muse and muse + J groups. Expression levels of BDNF and GDNF showed a marked decline in the PBS group. No significant change was seen with non-muse cell treatment, whereas the muse group displayed elevated expression. The expression remained unchanged in the muse + J group. (*Compared to the control group, ** P < 0.01, and compared to the PBS group, # P < 0.05, ## P < 0.01, & compared to the muse group, & P < 0.05) ( n = 3). C : The H&E staining results (200× magnification) showed that in the substantia nigra region of normal WT mice, the tissue structure was normal, and the cell nuclei were clearly visible (red arrows indicate astrocytes, green arrows indicate neuronal cells). In contrast, the brains of PBS group mice exhibited significant neuronal loss, with abnormal neuronal nuclear morphology and blurred boundaries. The non-muse group and muse + J group showed similar conditions to the PBS group, but the degree of neuronal damage was reduced. In the muse group, the number of damaged neurons was significantly decreased, and the tissue characteristics were similar to those of normal WT mice. (red→astrocyte, green→neuronal cells, black→damaged neuronal cells) ( n = 6)

Techniques Used: Staining, Labeling, Expressing, Western Blot, Control

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Journal: Journal of Translational Medicine

Article Title: Intranasally administered muse cells attenuate neurodegeneration in Parkinson’s disease

doi: 10.1186/s12967-025-07401-6

Figure Lengend Snippet: Muse cell has protective effects on DA neurons. A : (200×magnification) Compared to normal WT mice, the PBS group showed reduced TH and NeuN staining in the SNc region. In contrast to the PBS group, the muse group exhibited a higher number of TH-positive cells and NeuN-positive cells, with PKH26-labeled muse cells present in the region. Compared to the muse group, the muse + J and non-muse groups displayed relatively fewer TH-positive cells( n = 6). B : S1P expression in the brain tissue of A53T mice (PBS group) was significantly increased compared with normal WT mice. In the group treated with muse cells, S1P expression was markedly reduced relative to both the PBS and non-muse groups, though it remained higher than that in normal WT mice. Western blot results indicated: TNF-α expression in the brains of the PBS group was significantly higher than in control. Compared to the PBS group, TNF-α expression was significantly reduced in the muse group, while the non-muse and muse + J groups also showed reduced TNF-α expression. TNF-α expression in the muse group was lower than in the non-muse and muse + J groups. Expression levels of BDNF and GDNF showed a marked decline in the PBS group. No significant change was seen with non-muse cell treatment, whereas the muse group displayed elevated expression. The expression remained unchanged in the muse + J group. (*Compared to the control group, ** P < 0.01, and compared to the PBS group, # P < 0.05, ## P < 0.01, & compared to the muse group, & P < 0.05) ( n = 3). C : The H&E staining results (200× magnification) showed that in the substantia nigra region of normal WT mice, the tissue structure was normal, and the cell nuclei were clearly visible (red arrows indicate astrocytes, green arrows indicate neuronal cells). In contrast, the brains of PBS group mice exhibited significant neuronal loss, with abnormal neuronal nuclear morphology and blurred boundaries. The non-muse group and muse + J group showed similar conditions to the PBS group, but the degree of neuronal damage was reduced. In the muse group, the number of damaged neurons was significantly decreased, and the tissue characteristics were similar to those of normal WT mice. (red→astrocyte, green→neuronal cells, black→damaged neuronal cells) ( n = 6)

Article Snippet: GDNF Polyclonal antibody , 26179-1-AP , Proteintech.

Techniques: Staining, Labeling, Expressing, Western Blot, Control

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)

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)

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)

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)

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)

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)

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

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

CLDN11 is required for spermatogenesis in mice. a Appearance and weight of testes from Cldn11 +/+ , Cldn11 +/- , and Cldn11 -/- mice. The number of biologically independent mice in each group is shown as n in the graph. Data are shown as mean ± SD and were analyzed by Dunnett’s test. b , c Hematoxylin and eosin staining of sections prepared from testes ( b ) and the cauda epididymides ( c ) of Cldn11 +/- and Cldn11 -/- mice. The black dotted square is the region shown in a high magnification image (High mag.). A black arrowhead indicates a Sertoli cell cluster. d , e Immunohistochemistry of testis sections prepared from Cldn11 +/- and Cldn11 -/- mice using anti-KIT and anti-WT1 antibodies ( d ) or anti-GFRA1 and anti-WT1 antibodies ( e ). Cells expressing KIT ( d ) or GFRA1 ( e ) in seminiferous tubules are shown by yellow arrowheads. The number of KIT + ( d ) or GFRA1 + ( e ) cells on seminiferous tubule sections from testes of Cldn11 +/- and Cldn11 -/- mice were normalized to the number of WT1 + Sertoli cells in the graph. A total of 228–247 seminiferous tubules on testis sections from three biologically independent Cldn11 +/- or Cldn11 -/- mice were analyzed. Data were analyzed by Mann–Whitney U test. n.s. (not significant): P > 0.05. ( f ) TUNEL assay using testis sections prepared from Cldn11 +/- and Cldn11 -/- mice. The number of TUNEL + cells per seminiferous tubule section was counted. A total of 541 or 709 seminiferous tubules on testis sections from four Cldn11 +/- or five Cldn11 -/- biologically independent mice, respectively, were analyzed. Data were analyzed by Mann–Whitney U test. ( g ) TUNEL assay with immunohistochemistry of testis sections from Cldn11 -/- mice using anti-VASA ( g 1 ), anti-SCP3 ( g 2 ), anti-KIT ( g 3 ), or anti-PLZF antibodies ( g 4 ). Insets are magnified images of the regions indicated by white dotted squares. Scale bars: 1 cm ( a ), 50 μm ( b – e , g ), 100 μm ( f ), and 10 μm ( g , inset).

Journal: bioRxiv

Article Title: Claudin-11 regulates immunological barrier formation and spermatogonial proliferation through stem cell factor

doi: 10.1101/2024.07.16.602181

Figure Lengend Snippet: CLDN11 is required for spermatogenesis in mice. a Appearance and weight of testes from Cldn11 +/+ , Cldn11 +/- , and Cldn11 -/- mice. The number of biologically independent mice in each group is shown as n in the graph. Data are shown as mean ± SD and were analyzed by Dunnett’s test. b , c Hematoxylin and eosin staining of sections prepared from testes ( b ) and the cauda epididymides ( c ) of Cldn11 +/- and Cldn11 -/- mice. The black dotted square is the region shown in a high magnification image (High mag.). A black arrowhead indicates a Sertoli cell cluster. d , e Immunohistochemistry of testis sections prepared from Cldn11 +/- and Cldn11 -/- mice using anti-KIT and anti-WT1 antibodies ( d ) or anti-GFRA1 and anti-WT1 antibodies ( e ). Cells expressing KIT ( d ) or GFRA1 ( e ) in seminiferous tubules are shown by yellow arrowheads. The number of KIT + ( d ) or GFRA1 + ( e ) cells on seminiferous tubule sections from testes of Cldn11 +/- and Cldn11 -/- mice were normalized to the number of WT1 + Sertoli cells in the graph. A total of 228–247 seminiferous tubules on testis sections from three biologically independent Cldn11 +/- or Cldn11 -/- mice were analyzed. Data were analyzed by Mann–Whitney U test. n.s. (not significant): P > 0.05. ( f ) TUNEL assay using testis sections prepared from Cldn11 +/- and Cldn11 -/- mice. The number of TUNEL + cells per seminiferous tubule section was counted. A total of 541 or 709 seminiferous tubules on testis sections from four Cldn11 +/- or five Cldn11 -/- biologically independent mice, respectively, were analyzed. Data were analyzed by Mann–Whitney U test. ( g ) TUNEL assay with immunohistochemistry of testis sections from Cldn11 -/- mice using anti-VASA ( g 1 ), anti-SCP3 ( g 2 ), anti-KIT ( g 3 ), or anti-PLZF antibodies ( g 4 ). Insets are magnified images of the regions indicated by white dotted squares. Scale bars: 1 cm ( a ), 50 μm ( b – e , g ), 100 μm ( f ), and 10 μm ( g , inset).

Article Snippet: The following primary antibodies were used: rat monoclonal anti-ZO1 (R26.4C; Developmental Studies Hybridoma Bank) ; mouse monoclonal anti-ZO1 (T8-754) ; rat monoclonal anti-OCLN (MOC37) ; rabbit polyclonal anti-OCLN ; rabbit polyclonal anti-CLDN3 (#34-1700; Thermo Fisher Scientific); rabbit polyclonal anti-CLDN5 (#34-1600; Thermo Fisher Scientific); rabbit polyclonal anti-CLDN11 ; rabbit polyclonal anti-CLDN11 (#ab53041; Abcam); rabbit polyclonal anti-JAM1 (#36-1700; Thermo Fisher Scientific); rat monoclonal anti-CDH1 (#M108; Takara); rat monoclonal anti-NECTIN2 (#ab16912; Abcam); rabbit polyclonal anti-GJA1 (#C6219; Sigma–Aldrich); rabbit polyclonal anti-EZR (#sc-20773; Santa Cruz Biotechnology); mouse monoclonal anti-ATP1A1 (#NB300-146; Novus Biologicals); goat polyclonal anti-GFRA1 (#AF560; R&D Systems); rabbit polyclonal anti-PLZF (#HPA001499; Sigma–Aldrich); goat polyclonal anti-LIN28A (#AF3757; R&D Systems); goat polyclonal anti-KIT (#AF1356; R&D Systems); rabbit polyclonal anti-SCP3 (#ab15093; Abcam); rabbit polyclonal anti-VASA (#ab13840; Abcam); rabbit monoclonal anti-WT1 (#ab89901; Abcam); rabbit polyclonal anti-SCF (#ab64677; Abcam; characterized in Supplementary Fig. 13d, e); rabbit polyclonal anti-Ki67 (#ab15580; Abcam); rat monoclonal anti-CD45 (#103101; BioLegend); rabbit polyclonal anti-HA (#561; MBL); and mouse monoclonal anti-α-tubulin (#T6199; Sigma–Aldrich).

Techniques: Staining, Immunohistochemistry, Expressing, MANN-WHITNEY, TUNEL Assay

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.

Techniques: Permeability, Derivative Assay, Expressing, Control

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