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aluminum hydroxide  (InvivoGen)


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    Structured Review

    InvivoGen aluminum hydroxide
    Aluminum Hydroxide, supplied by InvivoGen, used in various techniques. Bioz Stars score: 99/100, based on 1095 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/aluminum+hydroxide/Alhydrogel+adjuvant+2%25/pm42262867-204-24-30
    Average 99 stars, based on 1095 article reviews
    aluminum hydroxide - by Bioz Stars, 2026-09
    99/100 stars

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    Related Articles

    Vaccines:

    Article Title: Lipidated Protein D vaccination elicits humoral and cellular responses and protects mice against challenge with non-typeable Haemophilus influenzae .
    Article Snippet: .. Vaccines consisted of 10 μg L-PD or NL-PD with or without 200 μg aluminum hydroxide (Alhydrogel, Invivogen) formulated in Tris-buffered saline containing 0.05% zwittergent 3-14. ..

    Saline:

    Article Title: Lipidated Protein D vaccination elicits humoral and cellular responses and protects mice against challenge with non-typeable Haemophilus influenzae .
    Article Snippet: .. Vaccines consisted of 10 μg L-PD or NL-PD with or without 200 μg aluminum hydroxide (Alhydrogel, Invivogen) formulated in Tris-buffered saline containing 0.05% zwittergent 3-14. ..

    Article Title: Helminth infection modulates the immunogenicity of COVID-19 vaccines in mice without compromising protective efficacy
    Article Snippet: .. Briefly, the alum-adjuvanted spike protein vaccine was prepared by mixing 25 μL of 10 mg/mL aluminum hydroxide (Alhydrogel 2% gel, InvivoGen, USA) with 25 μL of saline solution, followed by vortexing at high speed for 5 s to obtain the alum adjuvant. ..

    Injection:

    Article Title: Preimmunization of SPF Mice With Capsid Virus-like Particle Has no Effect on CD8 + Immune Memory and Skin Inflammation in an Ovalbumin-Induced Dermatitis Model.
    Article Snippet: .. These mice were then sensitized with an intraperitoneal injection of 200 μL OVA/ alum solution containing 0.05 mg/mL ovalbumin (Albumin A5503; Sigma- Aldrich, St. Louis, Missouri, USA) and 1% aluminum hydroxide (Alhydrogel Adjuvant 2%; InvivoGen; Toulouse, France). .. Mice were offered snacks and had access to DietGelRecovery (ClearH2O; Westbrook, ME, USA) 3 days prior and 3 days postinjection to maintain body weight, which was obtained two consecutive days following sensitization.

    Article Title: Preimmunization of SPF Mice With Capsid Virus‐like Particle Has no Effect on CD8 + Immune Memory and Skin Inflammation in an Ovalbumin‐Induced Dermatitis Model
    Article Snippet: .. These mice were then sensitized with an intraperitoneal injection of 200 μL OVA/alum solution containing 0.05 mg/mL ovalbumin (Albumin A5503; Sigma‐Aldrich, St. Louis, Missouri, USA) and 1% aluminum hydroxide (Alhydrogel Adjuvant 2%; InvivoGen; Toulouse, France). ..

    Adjuvant:

    Article Title: Preimmunization of SPF Mice With Capsid Virus-like Particle Has no Effect on CD8 + Immune Memory and Skin Inflammation in an Ovalbumin-Induced Dermatitis Model.
    Article Snippet: .. These mice were then sensitized with an intraperitoneal injection of 200 μL OVA/ alum solution containing 0.05 mg/mL ovalbumin (Albumin A5503; Sigma- Aldrich, St. Louis, Missouri, USA) and 1% aluminum hydroxide (Alhydrogel Adjuvant 2%; InvivoGen; Toulouse, France). .. Mice were offered snacks and had access to DietGelRecovery (ClearH2O; Westbrook, ME, USA) 3 days prior and 3 days postinjection to maintain body weight, which was obtained two consecutive days following sensitization.

    Article Title: Preimmunization of SPF Mice With Capsid Virus‐like Particle Has no Effect on CD8 + Immune Memory and Skin Inflammation in an Ovalbumin‐Induced Dermatitis Model
    Article Snippet: .. These mice were then sensitized with an intraperitoneal injection of 200 μL OVA/alum solution containing 0.05 mg/mL ovalbumin (Albumin A5503; Sigma‐Aldrich, St. Louis, Missouri, USA) and 1% aluminum hydroxide (Alhydrogel Adjuvant 2%; InvivoGen; Toulouse, France). ..

    Article Title: Microbial metabolism of food allergens determines the severity of IgE-mediated anaphylaxis.
    Article Snippet: Article Microbial metabolism of food allergens determines the severity of IgE-mediated anaphylaxis

    Article Title: Helminth infection modulates the immunogenicity of COVID-19 vaccines in mice without compromising protective efficacy
    Article Snippet: .. Briefly, the alum-adjuvanted spike protein vaccine was prepared by mixing 25 μL of 10 mg/mL aluminum hydroxide (Alhydrogel 2% gel, InvivoGen, USA) with 25 μL of saline solution, followed by vortexing at high speed for 5 s to obtain the alum adjuvant. ..

    Article Title: Regulatory B cells contribute to allergen-encapsulating nanoparticle immunotherapy efficacy for food allergy.
    Article Snippet: .. In brief, on days 0 477 and 14, 4–6-week old mice were sensitized i.p. using 20 μg OVA adsorbed to 1 mg of 478 aluminum hydroxide (alum; Alhydrogel adjuvant 2%, Invivogen). ..

    Recombinant:

    Article Title: Microbial metabolism of food allergens determines the severity of IgE-mediated anaphylaxis.
    Article Snippet: Article Microbial metabolism of food allergens determines the severity of IgE-mediated anaphylaxis



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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Thermo Fisher buffer invitrogen a ry3488 fetal calf serum invitrogen 10091148 aluminum hydroxide aladdin a110531 bovine serum albumin bsa
    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Buffer Invitrogen A Ry3488 Fetal Calf Serum Invitrogen 10091148 Aluminum Hydroxide Aladdin A110531 Bovine Serum Albumin Bsa, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Zhiyuan Chemical Co Ltd aluminum hydroxide
    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
    Aluminum Hydroxide, supplied by Zhiyuan Chemical Co Ltd, 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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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. <t>OVA:</t> ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of <t>ACC</t> <t>injection</t> sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.
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    Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. OVA: ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of ACC injection sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Journal: Advanced Science

    Article Title: An Anterior Cingulate Cortex‐Anterior Insular Cortex Glutamatergic Circuit Gates Stress‐Induced Visceral Hypersensitivity and Anxiety via Ionotropic Glutamate Receptors Trafficking

    doi: 10.1002/advs.76298

    Figure Lengend Snippet: Inhibition of the ACC Glu ‐AIC Glu pathway fails to alleviate visceral hypersensitivity in a non‐mental stress model. (A,B) VMR to 40 and 60mmHg CRD stimulation. OVA: ovalbumin. Representative external abdominal oblique muscle EMG recordings in (A), analysis of the mean amplitude of △EMG in (B) (one‐way ANOVA test followed by Tukey's post‐hoc test, B, 40mmHg, F (2, 17) = 67.67, p < 0.0001; Kruskal–Wallis test followed by Dunnett's post‐hoc test, B, 60mmHg, p = 0.0003. (C) Schematic of bilateral rAAV virus injections in ACC of OVA rats. (D) Representative image of ACC injection sites. Scale bar, 200 µm. (E,F) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (E), statistical results in (F), Scale bar, 20 µm (unpaired Student's t ‐test, F, t (10) = 8.202, p < 0.0001). (G–J) Inhibition of ACC Glu relieves the visceral hypersensitivity induced by OVA. Representative external abdominal oblique muscle EMG recordings in (G), analysis of the mean amplitude of △EMG in (H–J) (Paired Student's t ‐test, H, 40mmHg, t (5) = 2.347, p = 0.0658; 60mmHg, t (5) = 0.2801, p = 0.7906; I, 40mmHg, t (5) = 4.486, p = 0.0065; 60mmHg, t (5) = 3.139, p = 0.0257; Unpaired Student's t ‐test, J, 40mmHg, t (10) = 7.46, p < 0.0001; 60mmHg, t (10) = 4.313, p = 0.0015. (K) Schematic of bilateral anterograde‐DIO (in ACC) and retrograde‐CRE (in AIC) virus injections in OVA rats. (L) Representative image of ACC injection sites. Scale bar, 200 µm. (M,N) C‐fos expression in ACC post‐virus injection. Representative images of colocalization in (M), statistical results in (N), Scale bar, 20 µm (unpaired Student's t ‐test, N, t (10) = 0.1144, p = 0.9112). (O‐R) Failure of ACC‐AIC circuit inhibition to reduce OVA‐induced visceral hypersensitivity. Representative external abdominal oblique muscle EMG recordings in (O), analysis of the mean amplitude of △EMG in (P‐R) (paired Student's t ‐test, P, 40mmHg, t (5) = 0.4976, p = 0.6399; 60mmHg, t (5) = 0.2252, p = 0.8308; Q, 40mmHg, t (5) = 0.9588, p = 0.3817; 60mmHg, t (5) = 0.7854, p = 0.4678; unpaired Student's t ‐test, R, 40mmHg, t (10) = 0.5248, p = 0.6111; 60mmHg, t (10) = 0.1117, p = 0.9132). Data presented as mean ± SEM ( n = 8 rats for the NC group and n = 6 rats for all other groups). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

    Article Snippet: Briefly, rats were sensitized to OVA by intraperitoneal injection of a solution containing OVA (100μg, MCE, Monmouth Junction, NJ, USA) as the antigen and aluminum hydroxide (10mg, MCE, Monmouth Junction, NJ, USA) as an adjuvant in 1mL saline.

    Techniques: Inhibition, Virus, Injection, Expressing