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nissl staining solution  (Beyotime)


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    Structured Review

    Beyotime nissl staining solution
    S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) <t>Immunohistochemistry</t> <t>staining</t> of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) <t>Nissl</t> staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.
    Nissl Staining Solution, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 1268 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/nissl+staining+solution/Nissl+Staining+Solution/pmc13099944-115-8-11
    Average 99 stars, based on 1268 article reviews
    nissl staining solution - by Bioz Stars, 2026-10
    99/100 stars

    Images

    1) Product Images from "Non-canonical role of “S6K1–SGK1” pathway in neuronal necroptosis following traumatic brain injury"

    Article Title: Non-canonical role of “S6K1–SGK1” pathway in neuronal necroptosis following traumatic brain injury

    Journal: Genes & Diseases

    doi: 10.1016/j.gendis.2025.101876

    S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) Immunohistochemistry staining of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) Nissl staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.
    Figure Legend Snippet: S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) Immunohistochemistry staining of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) Nissl staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.

    Techniques Used: Inhibition, Western Blot, Expressing, Knockdown, Immunohistochemistry, Staining, Injection, Immunofluorescence, Two Tailed Test

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    Incubation:

    Article Title: NDST3 suppression restores lysosomal acidification and ameliorates amyloid-β and MAPT/tau pathology in Alzheimer’s disease
    Article Snippet: .. The sections were then incubated in Nissl staining solution (#C0117, Beyotime) at room temperature for 15 min. ..

    Article Title: NDST3 suppression restores lysosomal acidification and ameliorates amyloid-β and MAPT/tau pathology in Alzheimer's disease.
    Article Snippet: .. The sections were then incubated in Nissl staining solution (#C0117, Beyotime) at room temperature for 15 min. ..

    Article Title: Clec7a promotes hippocampal microglial activation in rats with status epilepticus via inducing the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: Microglial polarization imbalance between pro-inflammatory M1 and anti-inflammatory M2 phenotypes is a key mechanism in epilepsy-related neuroinflammation.. This study explores the role of C-type lectin domain containing 7A (Clec7a) in M1 microglial polarization in epilepsy.. An AAV-shClec7a was injected intra-hippocampally into Sprague-Dawley rats prior to induction of status epilepticus (SE) using lithium-pilocarpine.

    Staining:

    Article Title: NDST3 suppression restores lysosomal acidification and ameliorates amyloid-β and MAPT/tau pathology in Alzheimer’s disease
    Article Snippet: .. The sections were then incubated in Nissl staining solution (#C0117, Beyotime) at room temperature for 15 min. ..

    Article Title: Non-canonical role of “S6K1–SGK1” pathway in neuronal necroptosis following traumatic brain injury
    Article Snippet: .. The brain sections were dewaxed and stained with Nissl staining solution (Beyotime) for 10 min. .. The stained brain sections were mounted on slides, covered by MMD, and examined under a microscope (Zeiss).

    Article Title: NDST3 suppression restores lysosomal acidification and ameliorates amyloid-β and MAPT/tau pathology in Alzheimer's disease.
    Article Snippet: .. The sections were then incubated in Nissl staining solution (#C0117, Beyotime) at room temperature for 15 min. ..

    Article Title: Propofol upregulates MFG-E8 in BV2 cells to inhibit pyroptosis mediated by the NF-κB/NLRP3 pathway, thereby ameliorating ischemic-reperfusion neuronal injury
    Article Snippet: .. The liquid was removed, and sections were exposed to Nissl staining solution (cat. no. C0117, Beyotime Institute of Biotechnology) for 10 min at 25°C. ..

    Article Title: Dexmedetomidine Improves BBB and Neuronal Damage in Subarachnoid Hemorrhage by Repressing S100A4-Mediated Astrocytic Reactivity
    Article Snippet: The number of apoptotic cells was analyzed via ImageJ software (version 2.9.0/1.53t) by a blinded observer. .. The brain sections were dewaxed in xylene, rehydrated with alcohol, and stained for 5 minutes with Nissl staining solution (catalog #C0117; Beyotime, China). ..

    Article Title: Clec7a promotes hippocampal microglial activation in rats with status epilepticus via inducing the TLR4/MyD88/NF-κB signaling pathway.
    Article Snippet: Microglial polarization imbalance between pro-inflammatory M1 and anti-inflammatory M2 phenotypes is a key mechanism in epilepsy-related neuroinflammation.. This study explores the role of C-type lectin domain containing 7A (Clec7a) in M1 microglial polarization in epilepsy.. An AAV-shClec7a was injected intra-hippocampally into Sprague-Dawley rats prior to induction of status epilepticus (SE) using lithium-pilocarpine.

    Article Title: Dexmedetomidine Improves BBB and Neuronal Damage in Subarachnoid Hemorrhage by Repressing S100A4-Mediated Astrocytic Reactivity.
    Article Snippet: The number of apoptotic cells was analyzed via ImageJ software (version 2.9.0/1.53t) by a blinded observer. .. The brain sections were dewaxed in xylene, rehydrated with alcohol, and stained for 5 minutes with Nissl staining solution (catalog #C0117; Beyotime, China). ..

    Article Title: Bindarit attenuates brain injury and neuroinflammation in status epilepticus by disrupting C3/C3aR signaling and modulating microglia-astrocyte interactions.
    Article Snippet: The relative intensity area of MAP2, GFAP, occludin, claudin-5, ZO-1, CD31, VCAM-1, C3, C3aR, SYP staining, and the number of cells with immunoreactivity of other above markers were analyzed using ImageJ software blindly by independent investigators. .. For Nissl staining, coronal hippocampal tissue sections were obtained and stained with Nissl staining solution (C0117, Beyotime, Hangzhou, China) for 10 min at room temperature. ..



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    S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) <t>Immunohistochemistry</t> <t>staining</t> of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) <t>Nissl</t> staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.
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    S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) <t>Immunohistochemistry</t> <t>staining</t> of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) <t>Nissl</t> staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.
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    Image Search Results


    S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) Immunohistochemistry staining of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) Nissl staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.

    Journal: Genes & Diseases

    Article Title: Non-canonical role of “S6K1–SGK1” pathway in neuronal necroptosis following traumatic brain injury

    doi: 10.1016/j.gendis.2025.101876

    Figure Lengend Snippet: S6K1 inhibition alleviates neuronal necroptosis through SGK1 following TBI in mice. (A, K) Western blotting showed increased expression of p-S6/S6, SGK1, p-MLKL/MLKL, and p-RIP3/RIP3 in the cortex following TBI. These changes were attenuated by S6K1 inhibitor treatment and S6K1 knockdown, as shown by decreased p-MLKL/MLKL and p-RIP3/RIP3 levels compared with the TBI group. (B–E, L, M) Statistical results of Western blotting. (F) Immunohistochemistry staining of p-S6K1 in the right cortex of mouse brain after TBI. Scale bar: 20 μm. (G) Statistical results of immunohistochemistry staining for the increased S6K1 expression. (H) Schematic illustration of protein detection and behavior paradigm following p-S6K1 inhibitor injection. (I) Nissl staining of decreased neurons after TBI, and increased neurons after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 20 μm. (J) Statistical results of Nissl staining for the numbers of neurons. (N) Enhanced immunofluorescence intensity of p-MLKL in the right cortex of mouse brain after TBI, and decreased immunofluorescence intensity after treatment with S6K1 inhibitor and knockdown compared with TBI. Scale bar: 50 μm. Two-tailed unpaired Student's t -test was used for (G). n = 3 or 4. ∗ P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, and ∗∗∗∗P < 0.0001 versus the Sham group. # P < 0.05 and ## P < 0.01 versus the TBI group.

    Article Snippet: The brain sections were dewaxed and stained with Nissl staining solution (Beyotime) for 10 min.

    Techniques: Inhibition, Western Blot, Expressing, Knockdown, Immunohistochemistry, Staining, Injection, Immunofluorescence, Two Tailed Test