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Waveform rescue and impairment of AIS in C9-MSNs (A) Example AP waveforms for Con-1 (blue) and C9-3 MSNs (black) before and after the addition of BK channel activator NS11021 (10 μM, lighter color shade). Scale bars, 20 mV, 10 ms. (B and C) Mean ± SEM AP amplitude, AHP, half-width, threshold, and rheobase of C9-3 MSNs in the presence and absence of NS11021, along with Con-1 MSNs, were examined in parallel. Statistics, ∗ p < 0.05 and ∗∗∗ p < 0.001, from paired t test or t test . Data: con-1: n = 8, N = 3. C9-3: n = 10, N = 4. (D) NS11021 treatment had no effect on AP output in C9-3 MSNs evoked from current stimulation. Con-1 patched in parallel, shown for reference. Data: Con-1: n = 8, N = 3. C9-3: n = 10, N = 4. Statistics, two-way repeated measures ANOVA followed by Tukey’s multiple comparisons test. (E) Images of Con-1 and C9-3 stained with AIS marker ankyrin-G, neuronal marker <t>MAP2,</t> and DAPI. Scale bars, 50 μm. (F) Mean ± SEM AIS length and distance of start of AIS from the cell soma. Data: Con-1: n = 16, N = 4. C9-3: n = 36, N = 4. ∗∗∗ p < 0.001, t test.
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Waveform rescue and impairment of AIS in C9-MSNs (A) Example AP waveforms for Con-1 (blue) and C9-3 MSNs (black) before and after the addition of BK channel activator NS11021 (10 μM, lighter color shade). Scale bars, 20 mV, 10 ms. (B and C) Mean ± SEM AP amplitude, AHP, half-width, threshold, and rheobase of C9-3 MSNs in the presence and absence of NS11021, along with Con-1 MSNs, were examined in parallel. Statistics, ∗ p < 0.05 and ∗∗∗ p < 0.001, from paired t test or t test . Data: con-1: n = 8, N = 3. C9-3: n = 10, N = 4. (D) NS11021 treatment had no effect on AP output in C9-3 MSNs evoked from current stimulation. Con-1 patched in parallel, shown for reference. Data: Con-1: n = 8, N = 3. C9-3: n = 10, N = 4. Statistics, two-way repeated measures ANOVA followed by Tukey’s multiple comparisons test. (E) Images of Con-1 and C9-3 stained with AIS marker ankyrin-G, neuronal marker <t>MAP2,</t> and DAPI. Scale bars, 50 μm. (F) Mean ± SEM AIS length and distance of start of AIS from the cell soma. Data: Con-1: n = 16, N = 4. C9-3: n = 36, N = 4. ∗∗∗ p < 0.001, t test.
Fitc Conjugated Rabbit Anti Mouse Map2 Primary Antibody, supplied by Wuhan Fine Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of <t>MAP2,</t> PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.
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Image Search Results


Waveform rescue and impairment of AIS in C9-MSNs (A) Example AP waveforms for Con-1 (blue) and C9-3 MSNs (black) before and after the addition of BK channel activator NS11021 (10 μM, lighter color shade). Scale bars, 20 mV, 10 ms. (B and C) Mean ± SEM AP amplitude, AHP, half-width, threshold, and rheobase of C9-3 MSNs in the presence and absence of NS11021, along with Con-1 MSNs, were examined in parallel. Statistics, ∗ p < 0.05 and ∗∗∗ p < 0.001, from paired t test or t test . Data: con-1: n = 8, N = 3. C9-3: n = 10, N = 4. (D) NS11021 treatment had no effect on AP output in C9-3 MSNs evoked from current stimulation. Con-1 patched in parallel, shown for reference. Data: Con-1: n = 8, N = 3. C9-3: n = 10, N = 4. Statistics, two-way repeated measures ANOVA followed by Tukey’s multiple comparisons test. (E) Images of Con-1 and C9-3 stained with AIS marker ankyrin-G, neuronal marker MAP2, and DAPI. Scale bars, 50 μm. (F) Mean ± SEM AIS length and distance of start of AIS from the cell soma. Data: Con-1: n = 16, N = 4. C9-3: n = 36, N = 4. ∗∗∗ p < 0.001, t test.

Journal: Cell Reports

Article Title: Striatal neuron dysfunction in C9ORF72-FTD/ALS is driven by AIS and potassium channel dysregulation

doi: 10.1016/j.celrep.2026.117672

Figure Lengend Snippet: Waveform rescue and impairment of AIS in C9-MSNs (A) Example AP waveforms for Con-1 (blue) and C9-3 MSNs (black) before and after the addition of BK channel activator NS11021 (10 μM, lighter color shade). Scale bars, 20 mV, 10 ms. (B and C) Mean ± SEM AP amplitude, AHP, half-width, threshold, and rheobase of C9-3 MSNs in the presence and absence of NS11021, along with Con-1 MSNs, were examined in parallel. Statistics, ∗ p < 0.05 and ∗∗∗ p < 0.001, from paired t test or t test . Data: con-1: n = 8, N = 3. C9-3: n = 10, N = 4. (D) NS11021 treatment had no effect on AP output in C9-3 MSNs evoked from current stimulation. Con-1 patched in parallel, shown for reference. Data: Con-1: n = 8, N = 3. C9-3: n = 10, N = 4. Statistics, two-way repeated measures ANOVA followed by Tukey’s multiple comparisons test. (E) Images of Con-1 and C9-3 stained with AIS marker ankyrin-G, neuronal marker MAP2, and DAPI. Scale bars, 50 μm. (F) Mean ± SEM AIS length and distance of start of AIS from the cell soma. Data: Con-1: n = 16, N = 4. C9-3: n = 36, N = 4. ∗∗∗ p < 0.001, t test.

Article Snippet: MAP2 anti-Rabbit (1:1000) , Synaptic Systems , Cat# 188 003; RRID AB_2281442.

Techniques: Staining, Marker

OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of MAP2, PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.

Journal: Frontiers in Pharmacology

Article Title: Oxymatrine alleviates cognitive dysfunction in mice caused by chronic cerebral hypoperfusion by promoting SIRT1/ PINK1-mediated mitophagy

doi: 10.3389/fphar.2026.1736022

Figure Lengend Snippet: OMT reversed the neurons damage and mitophagy reduction in the hippocampal of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of MAP2, PSD95 and SYN, n = 5; (C) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (D) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (E,F) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin.

Article Snippet: The antibodies of microtubule-associated protein 2 (MAP2, A2572), postsynaptic density protein-95 (PSD95, A6194), synaptophysin (SYN, A6344) and sirtuin 1 (SIRT1, A11267) were sourced from Abclonal Technology Co., Ltd., Wuhan, China.

Techniques: Immunofluorescence, Expressing, Electron Microscopy, Control

OMT restored the mitophagy reduction and the SIRT1 inhibition in the hippocampus of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of PINK1and PARKIN, n = 5; (C) The mRNA expression of PINK1and PARKIN, n = 6; (D) Binding energy of OMT with downstream targets and binding sites of OMT to SIRT1; (E,F) Representative immunofluorescence images and quantitative analysis (n = 5), mRNA expression (n = 6) of SIRT1; (G,H) The protein expression and quantitative analysis of PINK1, PARKIN and SIRT1, n = 3. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Journal: Frontiers in Pharmacology

Article Title: Oxymatrine alleviates cognitive dysfunction in mice caused by chronic cerebral hypoperfusion by promoting SIRT1/ PINK1-mediated mitophagy

doi: 10.3389/fphar.2026.1736022

Figure Lengend Snippet: OMT restored the mitophagy reduction and the SIRT1 inhibition in the hippocampus of CCH mice. (A,B) Representative immunofluorescence images and quantitative analysis of PINK1and PARKIN, n = 5; (C) The mRNA expression of PINK1and PARKIN, n = 6; (D) Binding energy of OMT with downstream targets and binding sites of OMT to SIRT1; (E,F) Representative immunofluorescence images and quantitative analysis (n = 5), mRNA expression (n = 6) of SIRT1; (G,H) The protein expression and quantitative analysis of PINK1, PARKIN and SIRT1, n = 3. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Article Snippet: The antibodies of microtubule-associated protein 2 (MAP2, A2572), postsynaptic density protein-95 (PSD95, A6194), synaptophysin (SYN, A6344) and sirtuin 1 (SIRT1, A11267) were sourced from Abclonal Technology Co., Ltd., Wuhan, China.

Techniques: Inhibition, Immunofluorescence, Expressing, Binding Assay, Control

OMT reversed the OGD/R induced HT22 cell dysfunction, mitophagy inhibition and decreased SIRT1 expression. (A) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (B) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (C) The mRNA expression of PINK1, PARKIN and SIRT1, n = 6; (D) The protein expression and quantitative analysis of PINK1, PARKIN and SIRT1, n = 3; (E) Detection of JC-1 aggregates (red) and monomers (green) by confocal fluorescence microscopy, 1000×, n = 3; (F) Colocalization of lysosome (green) and mitochondria (red) by confocal fluorescence microscopy, 400×, 1000×, n = 3; (G) Representative ROS images, 100×, n = 5. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Journal: Frontiers in Pharmacology

Article Title: Oxymatrine alleviates cognitive dysfunction in mice caused by chronic cerebral hypoperfusion by promoting SIRT1/ PINK1-mediated mitophagy

doi: 10.3389/fphar.2026.1736022

Figure Lengend Snippet: OMT reversed the OGD/R induced HT22 cell dysfunction, mitophagy inhibition and decreased SIRT1 expression. (A) The mRNA expression of MAP2, PSD95 and SYN, n = 6; (B) The protein expression and quantitative analysis of MAP2, PSD95 and SYN, n = 3; (C) The mRNA expression of PINK1, PARKIN and SIRT1, n = 6; (D) The protein expression and quantitative analysis of PINK1, PARKIN and SIRT1, n = 3; (E) Detection of JC-1 aggregates (red) and monomers (green) by confocal fluorescence microscopy, 1000×, n = 3; (F) Colocalization of lysosome (green) and mitochondria (red) by confocal fluorescence microscopy, 400×, 1000×, n = 3; (G) Representative ROS images, 100×, n = 5. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Article Snippet: The antibodies of microtubule-associated protein 2 (MAP2, A2572), postsynaptic density protein-95 (PSD95, A6194), synaptophysin (SYN, A6344) and sirtuin 1 (SIRT1, A11267) were sourced from Abclonal Technology Co., Ltd., Wuhan, China.

Techniques: Inhibition, Expressing, Fluorescence, Microscopy, Control

SIRT1 and mitophagy mediate the protective effect of OMT on OGD/R HT22 cells. (A) The mRNA expression of MAP2, PSD95, SYN PINK1 and PARKIN, n = 6; (B,C) The protein expression and quantitative analysis of MAP2, PSD95, SYN PINK1 and PARKIN, n = 3; (D) Detection of JC-1 aggregates (red) and monomers (green) by confocal fluorescence microscopy, 1000×, n = 3; (E) Colocalization of lysosome (green) and mitochondria (red) by confocal fluorescence microscopy, 400×, 1000×, n = 3; (F) Representative ROS images, 100×, n = 5. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Journal: Frontiers in Pharmacology

Article Title: Oxymatrine alleviates cognitive dysfunction in mice caused by chronic cerebral hypoperfusion by promoting SIRT1/ PINK1-mediated mitophagy

doi: 10.3389/fphar.2026.1736022

Figure Lengend Snippet: SIRT1 and mitophagy mediate the protective effect of OMT on OGD/R HT22 cells. (A) The mRNA expression of MAP2, PSD95, SYN PINK1 and PARKIN, n = 6; (B,C) The protein expression and quantitative analysis of MAP2, PSD95, SYN PINK1 and PARKIN, n = 3; (D) Detection of JC-1 aggregates (red) and monomers (green) by confocal fluorescence microscopy, 1000×, n = 3; (E) Colocalization of lysosome (green) and mitochondria (red) by confocal fluorescence microscopy, 400×, 1000×, n = 3; (F) Representative ROS images, 100×, n = 5. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Article Snippet: The antibodies of microtubule-associated protein 2 (MAP2, A2572), postsynaptic density protein-95 (PSD95, A6194), synaptophysin (SYN, A6344) and sirtuin 1 (SIRT1, A11267) were sourced from Abclonal Technology Co., Ltd., Wuhan, China.

Techniques: Expressing, Fluorescence, Microscopy, Control

SIRT1 mediates the neuroprotective effect and mitophagy of OMT on the hippocampus of CCH mice. (A,B) The representative traces and quantitative analysis in OFT, Y-maze and NOR test, n = 6; (C,D) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6; (E,F) The mRNA expression of MAP2, PSD95, SYN PINK1 and PARKIN, n = 6; (G,H) Representative immunofluorescence images and quantitative analysis of MAP2 and PINK1, n = 5; (I,J) The protein expression and quantitative analysis of MAP2, PSD95, SYN PINK1 and PARKIN, n = 3. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Journal: Frontiers in Pharmacology

Article Title: Oxymatrine alleviates cognitive dysfunction in mice caused by chronic cerebral hypoperfusion by promoting SIRT1/ PINK1-mediated mitophagy

doi: 10.3389/fphar.2026.1736022

Figure Lengend Snippet: SIRT1 mediates the neuroprotective effect and mitophagy of OMT on the hippocampus of CCH mice. (A,B) The representative traces and quantitative analysis in OFT, Y-maze and NOR test, n = 6; (C,D) The mass of mitochondria and the number of mitophagosomes observed by electron microscopy, n = 6; (E,F) The mRNA expression of MAP2, PSD95, SYN PINK1 and PARKIN, n = 6; (G,H) Representative immunofluorescence images and quantitative analysis of MAP2 and PINK1, n = 5; (I,J) The protein expression and quantitative analysis of MAP2, PSD95, SYN PINK1 and PARKIN, n = 3. Means ± S.E.M. * P < 0.05, ** P < 0.01 vs. the corresponding control. CCH, chronic cerebral hypoperfusion; OMT, oxymatrine; MAP2, microtubule-associated protein 2; PSD95, postsynaptic density protein-95; SYN, synaptophysin; PINK1, PTEN-induced kinase 1; PARKIN, parkinson disease protein 2; SIRT1, Sirtuin 1.

Article Snippet: The antibodies of microtubule-associated protein 2 (MAP2, A2572), postsynaptic density protein-95 (PSD95, A6194), synaptophysin (SYN, A6344) and sirtuin 1 (SIRT1, A11267) were sourced from Abclonal Technology Co., Ltd., Wuhan, China.

Techniques: Electron Microscopy, Expressing, Immunofluorescence, Control