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: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

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

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: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

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

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: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

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

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: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

Techniques: Activation Assay, Activity Assay, Staining, Control

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: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

Techniques: Activation Assay, Expressing, Western Blot, Control

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 effect of A2BR activation on the apoptosis and migration of HP-infected GES-1 cells was abolished by SB203580. HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 in the presence or absence of 5 μM SB203580. A. Flow cytometry was utilized to measure the apoptotic rate. B. The transwell assay was used to evaluate the migration ability. C. The metastasis of cells was determined using the wound healing assay (**p < 0.01 vs. control, ##p < 0.01 vs. HP, &&p < 0.01 vs. HP + BAY60-6583).

Article Snippet: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

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

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 effects of A2BR activation on oxidative stress in HP-infected GES-1 cells were abolished by SB203580. HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 in the presence or absence of 5 μM SB203580. 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 < 0.01 vs. HP, &&p < 0.01 vs. HP + BAY60-6583).

Article Snippet: In the HP group, GES-1 cells were infected with HP for 24 h. In the HP + BAY60-6583 group, HP-infected GES-1 cells were incubated with 10 μM BAY60-6583 (MCE, USA), an agonist of A2BR [ ], for 24 h. In the HP + PSB1115 group, HP-infected GES-1 cells were incubated with 25 nM PSB1115 (GlpBio, USA), an antagonist of A2BR [ ], for 24 h. Apoptosis analysis: Cells were seeded in 6-well plates and incubated with Annexin V-fluorescein isothiocyanate (556,547; BD Biosciences, USA), followed by the addition of propidium iodide.

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