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Image Search Results
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Effects of Aβ1-42 given by intracerebroventricular injection on passive avoidance performance in mice. Various doses of Aβ1-42 were injected and on day 1 post-injection, mice were subjected to the training trial; testing trials were conducted on day 2 and day 8 post-injection. Control animals were injected with Aβ42-1 (410 pmol per mouse). The data are expressed as mean±s.e.mean, with n=10 – 20 mice per group. ** P<0.01 compared to Aβ42-1-treated control.
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques: Injection
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Protective effect of ferulic acid on the Aβ1-42-induced impairment in learning and memory in mice. After injection of Aβ (410 pmol per mouse), each behavioural test was performed as shown in Figure 2. Passive avoidance task (a,b): On day 1 post-injection, mice were trained on a one-trial step-through passive avoidance task. The testing trial was given 1 day after the training trial. (a) Dose-dependent effect of ferulic acid. (b) Time-dependent effect of ferulic acid. Y-maze task: Spontaneous alternation behaviour (c) and the number of arm entries (d) were measured during an 8-min session. Water-maze task: The training trials (e) and probe trial (f) were carried out on days 1 – 5 and on day 6 after Aβ injection, respectively. The latency showed the mean of a block of three trials per day (e). The data are presented as means±s.e.mean (n=10 – 20). Control mice were injected with Aβ42-1 (410 pmol per mouse). * P<0.05, ** P<0.01, *** P<0.001 vs Aβ42-1-treated control, # P<0.05, ## P<0.01 vs Aβ1-42 alone.
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques: Injection, Blocking Assay
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Effect of ferulic acid on the Aβ1-42-induced decrease in acetylcholine levels. Mice were allowed free access to the drinking water containing ferulic acid (0.006%) for up to 4 weeks prior to 410 pmol Aβ1-42 or Aβ42-1 injection. Acetylcholine level in the cortex was measured on day 5 after Aβ injection. Control animals were injected with 410 pmol Aβ42-1. The data are means±s.e.mean (n=10). * P<0.05 vs Aβ42-1-treated control.
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques: Injection
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Blockade of the Aβ1-42-induced increase in GFAP and IL-1β immunoreactivity by ferulic acid. Mice were allowed free access to normal drinking water (a,b,d,e), or water containing ferulic acid (0.006%) (c,f) for up to 4 weeks prior to Aβ injection. GFAP (a – c) and IL-1β (d – f) immunoreactivities in the hippocampus were examined on day 5 after injection of 410 pmol Aβ42-1 (a,d) or Aβ1-42 (b,c,e,f). Mice injected with 410 pmol Aβ42-1 (a,d) served as controls. Scale bar, 100 μm.
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques: Injection
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Ferulic acid induces transient increase in GFAP and IL-1β immunoreactivities in hippocampus. Mice were allowed free access to water containing ferulic acid (0.006%) for 1 (b,g), 5 (c,h), 14 (d,i) and 28 (e,j) days before being examined for GFAP (a – e) and IL-1β (f – j) immunoreactivities in hippocampus. Mice not exposed to ferulic acid (a,f) served as controls. OML, outer molecular layer, DG, dentate gyrus. Scale bar, 50 μm.
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques:
Journal:
Article Title: Protection against ?-amyloid peptide toxicity in vivo with long-term administration of ferulic acid
doi: 10.1038/sj.bjp.0704047
Figure Lengend Snippet: Therapeutic effect of ferulic acid on the Aβ1-42-induced impairment in passive avoidance performance in mice. After injection of Aβ (410 pmol per mouse), ferulic acid was administered to mice after either immediately, 2 days, or 8 days after an i.c.v. injection of Aβ1-42. On day 28 post-injection, mice were trained on a one-trial step-through passive avoidance task. The testing trial was given 1 day after the training trial (a, Experimental schedule). The data are presented as means±s.e.mean (n=10 – 11). Control mice were injected with Aβ42-1 (410 pmol per mouse).
Article Snippet: After five 10-min rinses in PBS, sections were placed in cryoprotectant, pre-incubated for 30 min in 0.1 M PBS with 1% bovine serum albumin and 0.2% Triton X-100 and incubated overnight with the following primary antisera: rabbit anti-GFAP (1 : 2000; Chemicon) and
Techniques: Injection
Journal: Journal of Functional Foods
Article Title: Salidroside alleviates UVB-induced skin damage by inhibiting keratinocytes pyroptosis via the AQP3/ROS/GSDMD-N signaling pathway
doi: 10.1016/j.jff.2023.105647
Figure Lengend Snippet: Fig. 4. Salidroside (SAL) alleviates UVB induced inflammasome activation and reduces the release of inflammatory factors. (A) SAL inhibited the expressions of NLRP3, Caspase1, C-Caspase1 and GSDMD-N. (B) Concentration of IL-1β in supernatants of the culture media. (C) Concentration of IL-18 in supernatants of the culture media. All data were displayed as mean ± SEM, n = 5. *P < 0.05, **P < 0.01 versus group of UVB.
Article Snippet: The followings are the information of primary antibodies: rabbit anti-NLRP3 (Q96P20) mAb T55651 (1:1000, Abmart), rabbit anti-Caspase-1 (E9R2D) mAb #83383S (1:1000, CST), rabbit anti- C-Caspase-1 (Asp296) (E2G2I) Rabbit mAb #89332 (reactivity: mouse) (1:1000, CST), anti-C-Caspase-1 (Asp297) (D57A2) Rabbit mAb #4199(reactivity: human) (1:1000,CST), anti- Gasdermin D N terminal (P57764) (Q9D8T2) Rabbit mAb, PU224937(1:1000, abmart),
Techniques: Activation Assay, Concentration Assay
Journal: Journal of Functional Foods
Article Title: Salidroside alleviates UVB-induced skin damage by inhibiting keratinocytes pyroptosis via the AQP3/ROS/GSDMD-N signaling pathway
doi: 10.1016/j.jff.2023.105647
Figure Lengend Snippet: Fig. 5. Salidroside (SAL) suppresses pyroptosis via down-regulatin AQP3/ROS/GSDMD-N signaling pathway in HaCaT cell line. (A) The bands and analysis results of AQP3 expression in HaCaT cell line after the treatment of SAL. (B) The fluorescence results of the HaCaT cells with overexpression of AQP3. (C) The bands and analysis of AQP3 expression in HaCaT cell line after overexpression. (D) qPCR results of HaCaT with AQP3 overexpression and NC. (E) The concentration of H2O2 in cells. (F) The bands and analysis of Caspase1, C-Caspase1, NLRP3 and GSDMD-N after the overexpression of AQP3. (G) The concentration of IL-18 in cells after the overexpression of AQP3. (H) The concentration of IL-1β in cells after the overexpression of AQP3. (I) The level of ROS in cells after the overexpression of AQP3. (J) The inflammasomes in cells visualized by TEM. All data were displayed as mean ± SEM, n = 3. *P < 0.05, **P < 0.01 versus group of UVB; # P < 0.05, ##P < 0.01 versus group of AQP3+/+.
Article Snippet: The followings are the information of primary antibodies: rabbit anti-NLRP3 (Q96P20) mAb T55651 (1:1000, Abmart), rabbit anti-Caspase-1 (E9R2D) mAb #83383S (1:1000, CST), rabbit anti- C-Caspase-1 (Asp296) (E2G2I) Rabbit mAb #89332 (reactivity: mouse) (1:1000, CST), anti-C-Caspase-1 (Asp297) (D57A2) Rabbit mAb #4199(reactivity: human) (1:1000,CST), anti- Gasdermin D N terminal (P57764) (Q9D8T2) Rabbit mAb, PU224937(1:1000, abmart),
Techniques: Expressing, Fluorescence, Over Expression, Concentration Assay
Journal: Journal of Functional Foods
Article Title: Salidroside alleviates UVB-induced skin damage by inhibiting keratinocytes pyroptosis via the AQP3/ROS/GSDMD-N signaling pathway
doi: 10.1016/j.jff.2023.105647
Figure Lengend Snippet: Fig. 7. Salidroside (SAL) relieves UVB-induced oxidative damage and pyroptosis in mice (A) Immunohistochemical staining and analysis for AQP3. (B) The expression of AQP3 in the skin leision was dettected by Western blotting. (C) The concentrations of H2O2. (D) MDA, (E F) SOD, and GSH in skin lesions. (G) Immunohistochemistry staining and analysis for NLRP3. (H) The expressions of NLRP3, Caspase-1, C-Caspase-1, GSDMD-N, IL-1β and IL-18 were detected by Western blotting. All data were displayed as Mean ± SD, n = 3. *P < 0.05, **P < 0.01 versus group of UVB.
Article Snippet: The followings are the information of primary antibodies: rabbit anti-NLRP3 (Q96P20) mAb T55651 (1:1000, Abmart), rabbit anti-Caspase-1 (E9R2D) mAb #83383S (1:1000, CST), rabbit anti- C-Caspase-1 (Asp296) (E2G2I) Rabbit mAb #89332 (reactivity: mouse) (1:1000, CST), anti-C-Caspase-1 (Asp297) (D57A2) Rabbit mAb #4199(reactivity: human) (1:1000,CST), anti- Gasdermin D N terminal (P57764) (Q9D8T2) Rabbit mAb, PU224937(1:1000, abmart),
Techniques: Immunohistochemical staining, Staining, Expressing, Western Blot, Immunohistochemistry