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psb 1115  (Bio-Techne corporation)


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    Structured Review

    Bio-Techne corporation psb 1115
    Psb 1115, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 99/100, based on 549 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/psb 1115/product/Bio-Techne corporation
    Average 99 stars, based on 549 article reviews
    psb 1115 - by Bioz Stars, 2026-03
    99/100 stars

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    The apoptosis and migration of HP-infected GES-1 cells were facilitated by A2BR activation. A. The morphology of GES-1 cells was observed under an inverted microscope. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM <t>PSB1115.</t> B. Flow cytometry was utilized to measure the apoptotic rate. C. The transwell assay was used to evaluate the migration ability. D. The metastasis of cells was determined using the wound healing assay (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).
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    The apoptosis and migration of HP-infected GES-1 cells were facilitated by A2BR activation. A. The morphology of GES-1 cells was observed under an inverted microscope. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM <t>PSB1115.</t> B. Flow cytometry was utilized to measure the apoptotic rate. C. The transwell assay was used to evaluate the migration ability. D. The metastasis of cells was determined using the wound healing assay (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).
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    The apoptosis and migration of HP-infected GES-1 cells were facilitated by A2BR activation. A. The morphology of GES-1 cells was observed under an inverted microscope. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. B. Flow cytometry was utilized to measure the apoptotic rate. C. The transwell assay was used to evaluate the migration ability. D. The metastasis of cells was determined using the wound healing assay (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Journal: Heliyon

    Article Title: A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation

    doi: 10.1016/j.heliyon.2023.e21004

    Figure Lengend Snippet: The apoptosis and migration of HP-infected GES-1 cells were facilitated by A2BR activation. A. The morphology of GES-1 cells was observed under an inverted microscope. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. B. Flow cytometry was utilized to measure the apoptotic rate. C. The transwell assay was used to evaluate the migration ability. D. The metastasis of cells was determined using the wound healing assay (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Article Snippet: BAY60-6583 and SB203580 were purchased from MCE, while PSB1115 was purchased from GlpBio.

    Techniques: Migration, Infection, Activation Assay, Inverted Microscopy, Incubation, Flow Cytometry, Transwell Assay, Wound Healing Assay

    Oxidative stress in HP-infected GES-1 cells was aggravated by A2BR activation. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. A. The ROS level in GES-1 cells was evaluated by the DCFH-DA assay. B. The MDA level was determined by a commercial kit using the TBA method. C. SOD activity was checked by a commercial kit using the WST-1 method (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Journal: Heliyon

    Article Title: A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation

    doi: 10.1016/j.heliyon.2023.e21004

    Figure Lengend Snippet: Oxidative stress in HP-infected GES-1 cells was aggravated by A2BR activation. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. A. The ROS level in GES-1 cells was evaluated by the DCFH-DA assay. B. The MDA level was determined by a commercial kit using the TBA method. C. SOD activity was checked by a commercial kit using the WST-1 method (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Article Snippet: BAY60-6583 and SB203580 were purchased from MCE, while PSB1115 was purchased from GlpBio.

    Techniques: Infection, Activation Assay, Incubation, DCFH-DA Assay, Activity Assay

    P38MAPK signaling in HP-infected GES-1 cells was activated by A2BR activation. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. The expression levels of p38 and p-p38 were evaluated by Western blotting (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Journal: Heliyon

    Article Title: A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation

    doi: 10.1016/j.heliyon.2023.e21004

    Figure Lengend Snippet: P38MAPK signaling in HP-infected GES-1 cells was activated by A2BR activation. GES-1 cells were infected with HP, followed by incubation with 10 μM BAY60-6583 and 25 nM PSB1115. The expression levels of p38 and p-p38 were evaluated by Western blotting (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Article Snippet: BAY60-6583 and SB203580 were purchased from MCE, while PSB1115 was purchased from GlpBio.

    Techniques: Infection, Activation Assay, Incubation, Expressing, Western Blot

    The pathological state of gastric ulcers in HP-treated rats was aggravated by A2BR activation. Rats were treated with 2 mg/kg BAY60-6583 or 10 mg/kg PSB1115, followed by gastric ulcer modeling 30 min later. A. The ulcer area in each group was calculated. B. The pepsin activity in each group was determined using the stop-point assay of denatured hemoglobin hydrolysis. C. The pathological changes in gastric mucosa tissues were checked by the HE staining assay. D. The MDA level in gastric mucosa tissues was determined by a commercial kit using the TBA method. E. The SOD activity in gastric mucosa tissues was checked by a commercial kit using the WST-1 method (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Journal: Heliyon

    Article Title: A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation

    doi: 10.1016/j.heliyon.2023.e21004

    Figure Lengend Snippet: The pathological state of gastric ulcers in HP-treated rats was aggravated by A2BR activation. Rats were treated with 2 mg/kg BAY60-6583 or 10 mg/kg PSB1115, followed by gastric ulcer modeling 30 min later. A. The ulcer area in each group was calculated. B. The pepsin activity in each group was determined using the stop-point assay of denatured hemoglobin hydrolysis. C. The pathological changes in gastric mucosa tissues were checked by the HE staining assay. D. The MDA level in gastric mucosa tissues was determined by a commercial kit using the TBA method. E. The SOD activity in gastric mucosa tissues was checked by a commercial kit using the WST-1 method (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Article Snippet: BAY60-6583 and SB203580 were purchased from MCE, while PSB1115 was purchased from GlpBio.

    Techniques: Activation Assay, Activity Assay, Staining

    P38MAPK signaling in HP-treated rats was activated by A2BR activation. Rats were treated with 2 mg/kg BAY60-6583 or 10 mg/kg PSB1115, followed by gastric ulcer modeling 30 min later. The expression levels of p38 and p-p38 in gastric mucosal tissues were evaluated by Western blotting (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Journal: Heliyon

    Article Title: A2BR facilitates the pathogenesis of H. pylori-associated GU by inducing oxidative stress through p38 MAPK phosphorylation

    doi: 10.1016/j.heliyon.2023.e21004

    Figure Lengend Snippet: P38MAPK signaling in HP-treated rats was activated by A2BR activation. Rats were treated with 2 mg/kg BAY60-6583 or 10 mg/kg PSB1115, followed by gastric ulcer modeling 30 min later. The expression levels of p38 and p-p38 in gastric mucosal tissues were evaluated by Western blotting (**p < 0.01 vs. control, #p < 0.05 vs. HP, ##p < 0.01 vs. HP).

    Article Snippet: BAY60-6583 and SB203580 were purchased from MCE, while PSB1115 was purchased from GlpBio.

    Techniques: Activation Assay, Expressing, Western Blot