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mouse model of constipation  (Federation of European Neuroscience Societies)

 
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    Federation of European Neuroscience Societies mouse model of constipation
    Mouse Model Of Constipation, supplied by Federation of European Neuroscience Societies, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/mouse+model+of+constipation/mouse+model+of+constipation/pm35852037-69-9-19
    Average 90 stars, based on 1 article reviews
    mouse model of constipation - by Bioz Stars, 2026-09
    90/100 stars

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    Article Title: Editor Profile: Rudi Beyaert.
    Article Snippet: doi:10.1111/febs.16570 In this special interview series, we profile members of The FEBS Journal editorial board to highlight their research focus, perspectives on the journal and future directions in their field.. Rudi Beyaert is Full Professor in Molecular Biology at the Department of Biomedical Molecular Biology, Faculty of Sciences, of the University of Ghent (Belgium).. He also serves as Vice-Science Director of the Center for Inflammation Research of the VIB in Ghent, where he is heading the Unit of Molecular Signal Transduction in Inflammation.



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    Acacetin improves gastrointestinal motility <t>in</t> <t>loperamide‐induced</t> <t>constipation</t> model. A loperamide‐induced constipation model was established in mice, different doses of acacetin were administered to the mice by oral gavaging (YWL‐high: 50 mg/kg/day; YWL‐medium: 25 mg/kg/day; YWL‐low: 10 mg/kg/day). The following parameters were monitored in an activated charcoal test after fasting treatment. (A‐D) Defecation initiation time; Fecal pellet counts at 8 h; Fecal water content; and intestinal propulsion rates. (E) Small intestine length measurements. (F) Gastrointestinal transit rates determined by activated charcoal propulsion. N = 6 animals in each group. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
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    Acacetin improves gastrointestinal motility <t>in</t> <t>loperamide‐induced</t> <t>constipation</t> model. A loperamide‐induced constipation model was established in mice, different doses of acacetin were administered to the mice by oral gavaging (YWL‐high: 50 mg/kg/day; YWL‐medium: 25 mg/kg/day; YWL‐low: 10 mg/kg/day). The following parameters were monitored in an activated charcoal test after fasting treatment. (A‐D) Defecation initiation time; Fecal pellet counts at 8 h; Fecal water content; and intestinal propulsion rates. (E) Small intestine length measurements. (F) Gastrointestinal transit rates determined by activated charcoal propulsion. N = 6 animals in each group. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.
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    Acacetin improves gastrointestinal motility in loperamide‐induced constipation model. A loperamide‐induced constipation model was established in mice, different doses of acacetin were administered to the mice by oral gavaging (YWL‐high: 50 mg/kg/day; YWL‐medium: 25 mg/kg/day; YWL‐low: 10 mg/kg/day). The following parameters were monitored in an activated charcoal test after fasting treatment. (A‐D) Defecation initiation time; Fecal pellet counts at 8 h; Fecal water content; and intestinal propulsion rates. (E) Small intestine length measurements. (F) Gastrointestinal transit rates determined by activated charcoal propulsion. N = 6 animals in each group. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Journal: Neurogastroenterology and Motility

    Article Title: Acacetin Alleviates Loperamide‐Induced Functional Constipation by Inhibiting P53 ‐Mediated Apoptosis in Colonic Epithelial Cells

    doi: 10.1111/nmo.70298

    Figure Lengend Snippet: Acacetin improves gastrointestinal motility in loperamide‐induced constipation model. A loperamide‐induced constipation model was established in mice, different doses of acacetin were administered to the mice by oral gavaging (YWL‐high: 50 mg/kg/day; YWL‐medium: 25 mg/kg/day; YWL‐low: 10 mg/kg/day). The following parameters were monitored in an activated charcoal test after fasting treatment. (A‐D) Defecation initiation time; Fecal pellet counts at 8 h; Fecal water content; and intestinal propulsion rates. (E) Small intestine length measurements. (F) Gastrointestinal transit rates determined by activated charcoal propulsion. N = 6 animals in each group. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Article Snippet: A loperamide‐induced functional constipation mouse model was established using oral gavaging of loperamide hydrochloride (HY‐B0418A, MedChemExpress, Shanghai, China) suspension [ , ].

    Techniques:

    YWL extract and acacetin protect against loperamide‐induced apoptosis in colonic mucosal epithelial cells. (A) Cell viability after treatment with increasing doses of YWL extract. (B) Cell viability after treatment with increasing doses of acacetin. (C) Cell viability rescue by YWL extract and acacetin against loperamide‐induced toxicity. (D) TUNEL staining showing suppression of loperamide‐induced apoptosis by YWL and acacetin. (E) Immunoblots of cleaved caspase‐3 and Bax levels. (F) Immunoblots of phospho‐ and total P53 and AKT1 levels. (G) P53 transcriptional activity analysis. N = 3 independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Journal: Neurogastroenterology and Motility

    Article Title: Acacetin Alleviates Loperamide‐Induced Functional Constipation by Inhibiting P53 ‐Mediated Apoptosis in Colonic Epithelial Cells

    doi: 10.1111/nmo.70298

    Figure Lengend Snippet: YWL extract and acacetin protect against loperamide‐induced apoptosis in colonic mucosal epithelial cells. (A) Cell viability after treatment with increasing doses of YWL extract. (B) Cell viability after treatment with increasing doses of acacetin. (C) Cell viability rescue by YWL extract and acacetin against loperamide‐induced toxicity. (D) TUNEL staining showing suppression of loperamide‐induced apoptosis by YWL and acacetin. (E) Immunoblots of cleaved caspase‐3 and Bax levels. (F) Immunoblots of phospho‐ and total P53 and AKT1 levels. (G) P53 transcriptional activity analysis. N = 3 independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Article Snippet: A loperamide‐induced functional constipation mouse model was established using oral gavaging of loperamide hydrochloride (HY‐B0418A, MedChemExpress, Shanghai, China) suspension [ , ].

    Techniques: TUNEL Assay, Staining, Western Blot, Activity Assay

    Activating P53 signaling abrogates the protection of acacetin against loperamide‐induced apoptosis. (A) P53 transcriptional activity analysis after Nutlin‐3a treatment. (B) Immunoblotting of phospho‐P53 and phospho‐AKT1 levels. (C) Cell viability analysis by CCK‐8 assay showing abrogation of the protective effect of acacetin by Nutlin‐3a. (D) TUNEL staining demonstrating Nutlin‐3a abolishes the suppression of acacetin on loperamide‐induced apoptosis. N = 3 independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Journal: Neurogastroenterology and Motility

    Article Title: Acacetin Alleviates Loperamide‐Induced Functional Constipation by Inhibiting P53 ‐Mediated Apoptosis in Colonic Epithelial Cells

    doi: 10.1111/nmo.70298

    Figure Lengend Snippet: Activating P53 signaling abrogates the protection of acacetin against loperamide‐induced apoptosis. (A) P53 transcriptional activity analysis after Nutlin‐3a treatment. (B) Immunoblotting of phospho‐P53 and phospho‐AKT1 levels. (C) Cell viability analysis by CCK‐8 assay showing abrogation of the protective effect of acacetin by Nutlin‐3a. (D) TUNEL staining demonstrating Nutlin‐3a abolishes the suppression of acacetin on loperamide‐induced apoptosis. N = 3 independent experiments. * p < 0.05; ** p < 0.01; *** p < 0.001; **** p < 0.0001.

    Article Snippet: A loperamide‐induced functional constipation mouse model was established using oral gavaging of loperamide hydrochloride (HY‐B0418A, MedChemExpress, Shanghai, China) suspension [ , ].

    Techniques: Activity Assay, Western Blot, CCK-8 Assay, TUNEL Assay, Staining