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anti murf1 monoclonal antibody  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology anti murf1 monoclonal antibody
    Anti Murf1 Monoclonal Antibody, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 430 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/anti+murf1/MuRF1+Antibody/pm41855087-49-5-18
    Average 96 stars, based on 430 article reviews
    anti murf1 monoclonal antibody - by Bioz Stars, 2026-10
    96/100 stars

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    Related Articles

    other:

    Article Title: Deferoxamine prevents dexamethasone-induced muscle atrophy by reducing MuRF1 and atrogin-1
    Article Snippet: Anti-GDF8 (sc134345), anti-KLF15 (sc271675), anti-MuRF1 (sc398608), anti-Ubiquitin (sc8017) antibodies were obtained from Santa Cruz Biotechnology (Dallas, TX, USA).

    Western Blot:

    Article Title: MuRF1 Partners With TRIM72 to Impair Insulin Signaling in Skeletal Muscle Cells
    Article Snippet: .. The following antibodies were applied for western blot analysis: Anti‐MuRF1 (Santa Cruz SC‐398608; 1:1000), Anti‐TRIM72 ( Antibodies.com A84884; 1:8000), Anti‐phospho Akt (Ser473) (Cell Signaling Technology 4060; 1:1000), Anti‐phospho‐Akt (T308) (Cell Signaling Technology 2965; 1:1000), Anti‐phospho‐P70 S6K1 (T389) (Cell Signaling Technology 9234; 1:1000), Anti‐GAPDH (Cell Signaling Technology 5174; 1:1000), Anti‐IRS1 (Cell Signaling Technology 3407; 1:1000), Anti‐GFP (Chromotek 3H9‐100; 1:2000), Anti‐FLAG M2 (Sigma‐Aldrich F1804; 1:1000), Anti‐Vinculin (Abcam ab73412; 1:1000), Anti‐Myosin (fast) (Sigma M4276; 1:1000), Anti‐PAX7 antibody (ThermoFisher; PA1‐117, 1:1000), and Anti‐Myosin (Slow) (Sigma M8421; 1:1000). .. The following secondary HRP‐linked antibodies were applied: Anti‐goat (Cell Signaling Technology 7077; 1:10000), Anti‐mouse (Cell Signaling Technology 7076; 1:10000), Anti‐rabbit (Cell Signaling Technology 7074; 1:10000), and Anti‐rat (Cell Signaling Technology 7077; 1:5000) antibodies.

    Article Title: Hydroxyethylamine & phthalimide analogs restoring defects due to GNE dysfunction: rare disease therapeutic significance
    Article Snippet: Primary antibodies for anti-LC3A/B (CST, Cat no. 4108 S) and anti-p62 (CST, Cat no. 5114 S), were purchased from Cell Signaling Technology, USA. .. Anti-Murf1 (sc-398608), anti-GAPDH (sc-32233), and HRP conjugated secondary antibodies for immunoblotting were purchased from Santa Cruz Biotechnology, USA. .. Alexa Fluor tagged secondary antibodies were purchased from Invitrogen, USA.

    Article Title: <scp>MuRF1</scp> Partners With <scp>TRIM72</scp> to Impair Insulin Signaling in Skeletal Muscle Cells
    Article Snippet: .. The following antibodies were applied for western blot analysis: Anti- MuRF1 (Santa Cruz SC- 398608; 1:1000), AntiTRIM72 (Antib odies. com A84884; 1:8000), Anti- phospho Akt (Ser473) (Cell Signaling Technology 4060; 1:1000), Antiphospho- Akt (T308) (Cell Signaling Technology 2965; 1:1000), Anti- phospho- P70 S6K1 (T389) (Cell Signaling Technology 9234; 1:1000), Anti- GAPDH (Cell Signaling Technology 5174; 1:1000), Anti- IRS1 (Cell Signaling Technology 3407; 1:1000), Anti- GFP (Chromotek 3H9- 100; 1:2000), Anti- FLAG M2 (Sigma- Aldrich F1804; 1:1000), Anti- Vinculin (Abcam ab73412; 1:1000), Anti- Myosin (fast) (Sigma M4276; 1:1000), Anti- PAX7 antibody (ThermoFisher; PA1- 117, 1:1000), and nloaded from https://faseb.onlinelibrary.w iley.com /doi/10.1096/fj.202502066R R by IN A SP - N E PA L , W iley O nline L ibrary on [13/11/2025]. .. See the T erm s and C onditions (https://onlinelibrary.w iley.com /term s-and-conditions) on W iley O nline L ibrary for rules of use; O A articles are governed by the applicable C reative C om m ons L icense 3 of 12 Anti- Myosin (Slow) (Sigma M8421; 1:1000).

    Article Title: MuRF1 partners with TRIM72 to impair insulin signalling in skeletal muscle cells
    Article Snippet: .. The following antibodies were applied for western blot analysis: Anti-MuRF1 (Santa Cruz SC-398608; 1:1000), Anti-TRIM72 ( Antibodies.com A84884; 1:8000), Anti-phospho Akt (Ser473) (Cell Signalling Technology 4060; 1:1000), Anti-phospho-Akt (T308) (Cell Signalling Technology 2965; 1:1000), Anti-phospho-P70 S6K1 (T389) (Cell Signalling Technology 9234; 1:1000), Anti-GAPDH (Cell Signalling Technology 5174; 1:1000), Anti IRS1 (Cell Signalling Technology 3407; 1:1000), Anti-GFP (Chromotek 3H9-100; 1:2000), Anti-FLAG M2 (Sigma-Aldrich F1804; 1:1000), Anti-Vinculin (Abcam ab73412; 1:1000), and Anti-puromycin (Sigma-Aldrich P8833; 1:1000). .. Anti-Myosin (fast) (Sigma M4276; 1:1000), Anti-PAX7 antibody (ThermoFisher; PA1-117, 1:1000), and Anti-Myosin (Slow) (Sigma M8421; 1:1000).

    Incubation:

    Article Title: A new mechanism of high-altitude adaptation reducing myocardium infarction: inhibiting inflammation-induced ubiquitin degradation of BK Ca to enhance coronary vasodilation.
    Article Snippet: Our prior research demonstrated that chronic intermittent hypobaric hypoxia (CIHH) pretreatment confers cardioprotection against ischemia/reperfusion (I/R) injury in rats.. However, the precise mechanisms underlying CIHH’s cardioprotective effects remain insufficiently understood.. This study aims to elucidate the upstream signaling pathways and dynamic regulation of BKCa channels in mediating CIHH-induced cardioprotection through coronary artery vasodilation in rats.

    Article Title: The therapeutic potential of Myoki, a novel peptide in muscle atrophy: mechanisms and applications
    Article Snippet: Each 20 μg sample was separated using 10% SDS–PAGE and transferred onto a polyvinylidene fluoride membrane (Millipore, Burlington, MA, USA). .. Non-specific binding was blocked with 5% non-fat dry milk for 1 h. The membranes were incubated overnight with primary antibodies: Anti-Myf5 (Abcam, ab125078), Anti-Myf6 (Abcam, ab182842), Anti-MyoD (Santa Cruz, sc-377460), Anti-MyoG (Santa Cruz, sc-52903), Anti-α-actinin (Santa Cruz, sc-17829), Anti-MYH3 (Santa Cruz, sc-53091), Anti-p-mTOR (Ser2448) (CST, #5536), Anti-p-Akt (Ser473) (CST, #9271), Anti-p-p70 S6 Kinase (Thr389) (CST, #9205), Anti-myostatin (Abcam, ab124721), Anti-atrogin-1/MAFbx (Santa Cruz, sc-166806), and Anti-MuRF1 (Santa Cruz, sc-398608). ..

    Binding Assay:

    Article Title: The therapeutic potential of Myoki, a novel peptide in muscle atrophy: mechanisms and applications
    Article Snippet: Each 20 μg sample was separated using 10% SDS–PAGE and transferred onto a polyvinylidene fluoride membrane (Millipore, Burlington, MA, USA). .. Non-specific binding was blocked with 5% non-fat dry milk for 1 h. The membranes were incubated overnight with primary antibodies: Anti-Myf5 (Abcam, ab125078), Anti-Myf6 (Abcam, ab182842), Anti-MyoD (Santa Cruz, sc-377460), Anti-MyoG (Santa Cruz, sc-52903), Anti-α-actinin (Santa Cruz, sc-17829), Anti-MYH3 (Santa Cruz, sc-53091), Anti-p-mTOR (Ser2448) (CST, #5536), Anti-p-Akt (Ser473) (CST, #9271), Anti-p-p70 S6 Kinase (Thr389) (CST, #9205), Anti-myostatin (Abcam, ab124721), Anti-atrogin-1/MAFbx (Santa Cruz, sc-166806), and Anti-MuRF1 (Santa Cruz, sc-398608). ..



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    Maslinic acid modulates atrophy-related marker expression in palmitic acid-treated C2C12 myotubes. Differentiated C2C12 myotubes were treated with MA (0-10 μM) and then challenged with PA (0.4 mM) under lipotoxic stress conditions. (A) Protein expression of myosin IIa, <t>MuRF1,</t> and Atrogin-1 was determined by Western blot analysis; GAPDH served as the internal control. (B-D) Immunofluorescence staining of (B) myosin IIa (green), (C) MuRF1 (green), and (D) Atrogin-1 (green) in differentiated C2C12 myotubes (200× original magnification); scale bar=50 μm. Nuclei were counterstained with DAPI (blue). Data are presented as mean ± SEM from three independent experiments. * p <0.05, ** p <0.01 vs. the PA group.
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    Maslinic acid modulates atrophy-related marker expression in palmitic acid-treated C2C12 myotubes. Differentiated C2C12 myotubes were treated with MA (0-10 μM) and then challenged with PA (0.4 mM) under lipotoxic stress conditions. (A) Protein expression of myosin IIa, <t>MuRF1,</t> and Atrogin-1 was determined by Western blot analysis; GAPDH served as the internal control. (B-D) Immunofluorescence staining of (B) myosin IIa (green), (C) MuRF1 (green), and (D) Atrogin-1 (green) in differentiated C2C12 myotubes (200× original magnification); scale bar=50 μm. Nuclei were counterstained with DAPI (blue). Data are presented as mean ± SEM from three independent experiments. * p <0.05, ** p <0.01 vs. the PA group.
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    Effects of VSE on inflammation-induced muscle atrophy in C2C12 myotubes. All experiments were carried out after C2C12 myoblasts had differentiated into myotubes for 4 days. C2C12 myotubes were pretreated with 0 (LPS only), 1.25, 2.5 or 5 µg/ml VSE for 3 h and then co-treated with 500 ng/ml LPS for (B, D and E) 24 h and (C) 48 h. Controls received no treatments. (A) C2C12 myotubes were exposed to 0–10 µg/ml VSE for 48 h to assess cytotoxicity. (B) mRNA levels of muscle-specific E3 ubiquitin ligases <t>MuRF1</t> and atrogin-1 were measured using reverse transcription-quantitative PCR. (C) Giemsa-stained images of C2C12 myotubes showing changes in relative fiber width after treatment. CON, untreated control; LPS, 500 ng/ml; 1.25, 2.5 and 5, co-treatment with LPS (500 ng/ml) and VSE at the indicated concentrations (µg/ml). Analysis was performed using ImageJ (National Institutes of Health). Scale bar, 100 µm. Western blot analysis of (D) MuRF1, MaFbx and MyHC protein levels, and (E) phosphorylated Akt and Foxo3a, including membrane images and semi-quantitative analysis using ImageJ. All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA with Tukey's post hoc test. ## P<0.01 and #### P<0.0001 vs. control group; *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001 vs. LPS-treated group. MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; CON, control; LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; p-, phosphorylated; ns, not significant.
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    Santa Cruz Biotechnology anti murf1 monoclonal antibody
    Effects of VSE on inflammation-induced muscle atrophy in C2C12 myotubes. All experiments were carried out after C2C12 myoblasts had differentiated into myotubes for 4 days. C2C12 myotubes were pretreated with 0 (LPS only), 1.25, 2.5 or 5 µg/ml VSE for 3 h and then co-treated with 500 ng/ml LPS for (B, D and E) 24 h and (C) 48 h. Controls received no treatments. (A) C2C12 myotubes were exposed to 0–10 µg/ml VSE for 48 h to assess cytotoxicity. (B) mRNA levels of muscle-specific E3 ubiquitin ligases <t>MuRF1</t> and atrogin-1 were measured using reverse transcription-quantitative PCR. (C) Giemsa-stained images of C2C12 myotubes showing changes in relative fiber width after treatment. CON, untreated control; LPS, 500 ng/ml; 1.25, 2.5 and 5, co-treatment with LPS (500 ng/ml) and VSE at the indicated concentrations (µg/ml). Analysis was performed using ImageJ (National Institutes of Health). Scale bar, 100 µm. Western blot analysis of (D) MuRF1, MaFbx and MyHC protein levels, and (E) phosphorylated Akt and Foxo3a, including membrane images and semi-quantitative analysis using ImageJ. All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA with Tukey's post hoc test. ## P<0.01 and #### P<0.0001 vs. control group; *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001 vs. LPS-treated group. MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; CON, control; LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; p-, phosphorylated; ns, not significant.
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    Santa Cruz Biotechnology murf1
    Effects of VSE on inflammation-induced muscle atrophy in C2C12 myotubes. All experiments were carried out after C2C12 myoblasts had differentiated into myotubes for 4 days. C2C12 myotubes were pretreated with 0 (LPS only), 1.25, 2.5 or 5 µg/ml VSE for 3 h and then co-treated with 500 ng/ml LPS for (B, D and E) 24 h and (C) 48 h. Controls received no treatments. (A) C2C12 myotubes were exposed to 0–10 µg/ml VSE for 48 h to assess cytotoxicity. (B) mRNA levels of muscle-specific E3 ubiquitin ligases <t>MuRF1</t> and atrogin-1 were measured using reverse transcription-quantitative PCR. (C) Giemsa-stained images of C2C12 myotubes showing changes in relative fiber width after treatment. CON, untreated control; LPS, 500 ng/ml; 1.25, 2.5 and 5, co-treatment with LPS (500 ng/ml) and VSE at the indicated concentrations (µg/ml). Analysis was performed using ImageJ (National Institutes of Health). Scale bar, 100 µm. Western blot analysis of (D) MuRF1, MaFbx and MyHC protein levels, and (E) phosphorylated Akt and Foxo3a, including membrane images and semi-quantitative analysis using ImageJ. All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA with Tukey's post hoc test. ## P<0.01 and #### P<0.0001 vs. control group; *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001 vs. LPS-treated group. MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; CON, control; LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; p-, phosphorylated; ns, not significant.
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    Image Search Results


    Maslinic acid modulates atrophy-related marker expression in palmitic acid-treated C2C12 myotubes. Differentiated C2C12 myotubes were treated with MA (0-10 μM) and then challenged with PA (0.4 mM) under lipotoxic stress conditions. (A) Protein expression of myosin IIa, MuRF1, and Atrogin-1 was determined by Western blot analysis; GAPDH served as the internal control. (B-D) Immunofluorescence staining of (B) myosin IIa (green), (C) MuRF1 (green), and (D) Atrogin-1 (green) in differentiated C2C12 myotubes (200× original magnification); scale bar=50 μm. Nuclei were counterstained with DAPI (blue). Data are presented as mean ± SEM from three independent experiments. * p <0.05, ** p <0.01 vs. the PA group.

    Journal: Biomolecules & Therapeutics

    Article Title: Maslinic Acid Alleviates Obesity-Associated Skeletal Muscle Atrophy and Adipose Tissue Dysfunction in Obese Mice

    doi: 10.4062/biomolther.2026.072

    Figure Lengend Snippet: Maslinic acid modulates atrophy-related marker expression in palmitic acid-treated C2C12 myotubes. Differentiated C2C12 myotubes were treated with MA (0-10 μM) and then challenged with PA (0.4 mM) under lipotoxic stress conditions. (A) Protein expression of myosin IIa, MuRF1, and Atrogin-1 was determined by Western blot analysis; GAPDH served as the internal control. (B-D) Immunofluorescence staining of (B) myosin IIa (green), (C) MuRF1 (green), and (D) Atrogin-1 (green) in differentiated C2C12 myotubes (200× original magnification); scale bar=50 μm. Nuclei were counterstained with DAPI (blue). Data are presented as mean ± SEM from three independent experiments. * p <0.05, ** p <0.01 vs. the PA group.

    Article Snippet: The sections were incubated with primary antibodies (1:50) at 4°C overnight, followed by incubation with the corresponding secondary antibody for 1 h. Signals for MuRF1 (#MP3401; ECM Biosciences) and Atrogin-1 (ab168372; Abcam) were visualized using a DAB chromogenic substrate.

    Techniques: Marker, Expressing, Western Blot, Control, Immunofluorescence, Staining

    Maslinic acid modulates atrophy-related protein expression and GLUT4 expression in the skeletal muscle of obese mice. (A) Protein expression of pAKT, AKT, myosin IIa, MuRF1, and Atrogin-1 in gastrocnemius muscle was determined by Western blot analysis; GAPDH served as the internal control. (B) Immunofluorescence staining of GLUT4 (green) and (C) MuRF1 (green) in gastrocnemius muscle. (D) Immunohistochemical staining of MuRF1 (dark brown). (E) Immunofluorescence staining (red) and (F) immunohistochemical staining of Atrogin-1 (dark brown) in gastrocnemius muscle (100×original magnification); scale bar=50 μm. Nuclei in the immunofluorescence images were counterstained with DAPI (blue). Data are presented as mean ± SEM; n=12 per group. * p <0.05, ** p <0.01 vs. the HFD group.

    Journal: Biomolecules & Therapeutics

    Article Title: Maslinic Acid Alleviates Obesity-Associated Skeletal Muscle Atrophy and Adipose Tissue Dysfunction in Obese Mice

    doi: 10.4062/biomolther.2026.072

    Figure Lengend Snippet: Maslinic acid modulates atrophy-related protein expression and GLUT4 expression in the skeletal muscle of obese mice. (A) Protein expression of pAKT, AKT, myosin IIa, MuRF1, and Atrogin-1 in gastrocnemius muscle was determined by Western blot analysis; GAPDH served as the internal control. (B) Immunofluorescence staining of GLUT4 (green) and (C) MuRF1 (green) in gastrocnemius muscle. (D) Immunohistochemical staining of MuRF1 (dark brown). (E) Immunofluorescence staining (red) and (F) immunohistochemical staining of Atrogin-1 (dark brown) in gastrocnemius muscle (100×original magnification); scale bar=50 μm. Nuclei in the immunofluorescence images were counterstained with DAPI (blue). Data are presented as mean ± SEM; n=12 per group. * p <0.05, ** p <0.01 vs. the HFD group.

    Article Snippet: The sections were incubated with primary antibodies (1:50) at 4°C overnight, followed by incubation with the corresponding secondary antibody for 1 h. Signals for MuRF1 (#MP3401; ECM Biosciences) and Atrogin-1 (ab168372; Abcam) were visualized using a DAB chromogenic substrate.

    Techniques: Expressing, Western Blot, Control, Immunofluorescence, Staining, Immunohistochemical staining

    Proposed model summarizing the effects of maslinic acid on adipocyte metabolic dysfunction and skeletal muscle atrophic changes in obese mice. Maslinic acid (MA) reduced lipid accumulation and inflammation in adipose tissue, decreased M1 macrophage-associated marker expression, increased M2 macrophage-associated marker expression, and lowered TNF-α and IL-6 levels. In skeletal muscle and palmitic acid-treated C2C12 myotubes, MA increased AKT and FOXO1 phosphorylation and myosin IIa expression, while reducing MuRF1 and Atrogin-1 expression. MA was also associated with improved mitochondrial morphology and respiratory responses, increased mitofusin-2 expression, and reduced DRP1 phosphorylation. Collectively, these changes may contribute to the attenuation of obesity-associated skeletal muscle atrophic changes. Upward and downward arrows indicate increases and decreases, respectively.

    Journal: Biomolecules & Therapeutics

    Article Title: Maslinic Acid Alleviates Obesity-Associated Skeletal Muscle Atrophy and Adipose Tissue Dysfunction in Obese Mice

    doi: 10.4062/biomolther.2026.072

    Figure Lengend Snippet: Proposed model summarizing the effects of maslinic acid on adipocyte metabolic dysfunction and skeletal muscle atrophic changes in obese mice. Maslinic acid (MA) reduced lipid accumulation and inflammation in adipose tissue, decreased M1 macrophage-associated marker expression, increased M2 macrophage-associated marker expression, and lowered TNF-α and IL-6 levels. In skeletal muscle and palmitic acid-treated C2C12 myotubes, MA increased AKT and FOXO1 phosphorylation and myosin IIa expression, while reducing MuRF1 and Atrogin-1 expression. MA was also associated with improved mitochondrial morphology and respiratory responses, increased mitofusin-2 expression, and reduced DRP1 phosphorylation. Collectively, these changes may contribute to the attenuation of obesity-associated skeletal muscle atrophic changes. Upward and downward arrows indicate increases and decreases, respectively.

    Article Snippet: The sections were incubated with primary antibodies (1:50) at 4°C overnight, followed by incubation with the corresponding secondary antibody for 1 h. Signals for MuRF1 (#MP3401; ECM Biosciences) and Atrogin-1 (ab168372; Abcam) were visualized using a DAB chromogenic substrate.

    Techniques: Marker, Expressing, Phospho-proteomics

    Effects of VSE on inflammation-induced muscle atrophy in C2C12 myotubes. All experiments were carried out after C2C12 myoblasts had differentiated into myotubes for 4 days. C2C12 myotubes were pretreated with 0 (LPS only), 1.25, 2.5 or 5 µg/ml VSE for 3 h and then co-treated with 500 ng/ml LPS for (B, D and E) 24 h and (C) 48 h. Controls received no treatments. (A) C2C12 myotubes were exposed to 0–10 µg/ml VSE for 48 h to assess cytotoxicity. (B) mRNA levels of muscle-specific E3 ubiquitin ligases MuRF1 and atrogin-1 were measured using reverse transcription-quantitative PCR. (C) Giemsa-stained images of C2C12 myotubes showing changes in relative fiber width after treatment. CON, untreated control; LPS, 500 ng/ml; 1.25, 2.5 and 5, co-treatment with LPS (500 ng/ml) and VSE at the indicated concentrations (µg/ml). Analysis was performed using ImageJ (National Institutes of Health). Scale bar, 100 µm. Western blot analysis of (D) MuRF1, MaFbx and MyHC protein levels, and (E) phosphorylated Akt and Foxo3a, including membrane images and semi-quantitative analysis using ImageJ. All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA with Tukey's post hoc test. ## P<0.01 and #### P<0.0001 vs. control group; *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001 vs. LPS-treated group. MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; CON, control; LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; p-, phosphorylated; ns, not significant.

    Journal: Molecular Medicine Reports

    Article Title: Veronicastrum sibiricum (L.) Pennell extract alleviates inflammation-induced muscle atrophy through NLRP3 inflammasome regulation and mitochondrial function restoration

    doi: 10.3892/mmr.2026.13857

    Figure Lengend Snippet: Effects of VSE on inflammation-induced muscle atrophy in C2C12 myotubes. All experiments were carried out after C2C12 myoblasts had differentiated into myotubes for 4 days. C2C12 myotubes were pretreated with 0 (LPS only), 1.25, 2.5 or 5 µg/ml VSE for 3 h and then co-treated with 500 ng/ml LPS for (B, D and E) 24 h and (C) 48 h. Controls received no treatments. (A) C2C12 myotubes were exposed to 0–10 µg/ml VSE for 48 h to assess cytotoxicity. (B) mRNA levels of muscle-specific E3 ubiquitin ligases MuRF1 and atrogin-1 were measured using reverse transcription-quantitative PCR. (C) Giemsa-stained images of C2C12 myotubes showing changes in relative fiber width after treatment. CON, untreated control; LPS, 500 ng/ml; 1.25, 2.5 and 5, co-treatment with LPS (500 ng/ml) and VSE at the indicated concentrations (µg/ml). Analysis was performed using ImageJ (National Institutes of Health). Scale bar, 100 µm. Western blot analysis of (D) MuRF1, MaFbx and MyHC protein levels, and (E) phosphorylated Akt and Foxo3a, including membrane images and semi-quantitative analysis using ImageJ. All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA with Tukey's post hoc test. ## P<0.01 and #### P<0.0001 vs. control group; *P < 0.05, **P < 0.01, *** P < 0.001, ****P < 0.0001 vs. LPS-treated group. MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; CON, control; LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; p-, phosphorylated; ns, not significant.

    Article Snippet: MuRF1 , Rabbit monoclonal , 4305 , Cell Signaling Technology, Inc. , 1:1,000.

    Techniques: Ubiquitin Proteomics, Reverse Transcription, Real-time Polymerase Chain Reaction, Staining, Control, Western Blot, Membrane

    VSE exhibits protective effects against pyroptosis. (A) Mouse serum was obtained 24 h after intraperitoneal LPS administration, diluted to 1:50, and the protein expression levels of proinflammatory cytokines TNF-α and IL-1β were analyzed using ELISAs. (B) GAS muscle tissue was obtained, the mRNA was extracted and the mRNA expression levels of muscle atrophy-related genes MuRF1 and atrogin-1 were analyzed using reverse transcription-quantitative PCR. (C) GAS muscle tissue was obtained, proteins were extracted utilizing PRO-PREP™, and the protein expression levels of muscle atrophy-related and NLRP3 pathway-related proteins were analyzed using western blotting (n=6 per group). All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA followed by Tukey's post hoc test in GraphPad Prism 10. ## P<0.01, ### P<0.001, #### P<0.0001 vs. control; *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. LPS treatment. LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; GAS, gastrocnemius; MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; NLRP3, NLR family pyrin domain containing 3; GSDMD, gasdermin-D; CON, control; A450, absorbance at 450 nm.

    Journal: Molecular Medicine Reports

    Article Title: Veronicastrum sibiricum (L.) Pennell extract alleviates inflammation-induced muscle atrophy through NLRP3 inflammasome regulation and mitochondrial function restoration

    doi: 10.3892/mmr.2026.13857

    Figure Lengend Snippet: VSE exhibits protective effects against pyroptosis. (A) Mouse serum was obtained 24 h after intraperitoneal LPS administration, diluted to 1:50, and the protein expression levels of proinflammatory cytokines TNF-α and IL-1β were analyzed using ELISAs. (B) GAS muscle tissue was obtained, the mRNA was extracted and the mRNA expression levels of muscle atrophy-related genes MuRF1 and atrogin-1 were analyzed using reverse transcription-quantitative PCR. (C) GAS muscle tissue was obtained, proteins were extracted utilizing PRO-PREP™, and the protein expression levels of muscle atrophy-related and NLRP3 pathway-related proteins were analyzed using western blotting (n=6 per group). All data are presented as the mean ± SD of triplicate results and statistical analysis was carried out using one-way ANOVA followed by Tukey's post hoc test in GraphPad Prism 10. ## P<0.01, ### P<0.001, #### P<0.0001 vs. control; *P<0.05, **P<0.01, ***P<0.001, ****P<0.0001 vs. LPS treatment. LPS, lipopolysaccharide; VSE, Veronicastrum sibiricum seed extract; GAS, gastrocnemius; MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein; MyHC, myosin heavy chain; NLRP3, NLR family pyrin domain containing 3; GSDMD, gasdermin-D; CON, control; A450, absorbance at 450 nm.

    Article Snippet: MuRF1 , Rabbit monoclonal , 4305 , Cell Signaling Technology, Inc. , 1:1,000.

    Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Control

    Schematic illustration of the VSE activation mechanism. VSE inhibits LPS-induced NLRP3 inflammasome activation and alleviates muscle atrophy through a reduction in the expression of E3 ligases. VSE, Veronicastrum sibiricum seed extract; LPS, lipopolysaccharide; ROS, reactive oxygen species; mtROS, mitochondrial reactive oxygen species; GSDMD, gasdermin-D; NLRP3, NLR family pyrin domain containing 3; MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein.

    Journal: Molecular Medicine Reports

    Article Title: Veronicastrum sibiricum (L.) Pennell extract alleviates inflammation-induced muscle atrophy through NLRP3 inflammasome regulation and mitochondrial function restoration

    doi: 10.3892/mmr.2026.13857

    Figure Lengend Snippet: Schematic illustration of the VSE activation mechanism. VSE inhibits LPS-induced NLRP3 inflammasome activation and alleviates muscle atrophy through a reduction in the expression of E3 ligases. VSE, Veronicastrum sibiricum seed extract; LPS, lipopolysaccharide; ROS, reactive oxygen species; mtROS, mitochondrial reactive oxygen species; GSDMD, gasdermin-D; NLRP3, NLR family pyrin domain containing 3; MuRF1, muscle-specific RING finger protein 1; MaFbx, muscle atrophy F-box protein.

    Article Snippet: MuRF1 , Rabbit monoclonal , 4305 , Cell Signaling Technology, Inc. , 1:1,000.

    Techniques: Activation Assay, Expressing