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Image Search Results
Journal: Journal of Neuroinflammation
Article Title: Curcumin reduces neuroinflammation and oxidative stress in a stroke model by epigenetically regulating ADRB2 methylation through JAK2/STAT3 and Nrf2/HO-1 pathways
doi: 10.1186/s12974-026-03729-y
Figure Lengend Snippet: ADRB2 gene is closely associated with inflammation in OGD/R-induced HBMECs. A Flowchart. B RT-qPCR validation of successful plasmid overexpression of ADRB2 . n = 15. C Representative Western blot bands for ADRB2 in HBMECs cell lysates following ADRB2 plasmid overexpression. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. D Density quantification of ADRB2 bands. n = 4. E RT-qPCR validation of successful ADRB2 knockdown using siRNA. n = 9. F Representative Western blot bands for ADRB2 in HBMECs cell lysates following ADRB2 knockdown with siRNA. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. G Density quantification of ADRB2 bands. n = 5. H Representative images of siRNA and plasmid transfection labeled with fluorescent vector. Green indicates successful transfection of siRNA and plasmid into cells. Scale bar, 1000 μm. I Representative Western blot bands for p-JAK2, JAK2, p-STAT3, STAT3, IL-1β, IL-6, and TNF-α in cell lysates from OGD/R-induced HBMECs treated with empty vector, ADRB2 knockdown siRNA, and ADRB2 overexpression plasmid. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. J - N Density quantification of IL-1β ( J ), IL-6 ( K ), TNF-α ( L ), p-JAK2 and JAK2 ( M ), p-STAT3 and STAT3. N . n = 6. O ELISA analysis of inflammatory cytokines IL-10 in the supernatants of OGD/R-induced HBMECs treated with empty vector, ADRB2 knockdown siRNA, and ADRB2 overexpression plasmid. n = 3. P Representative Western blot bands for ADRB2, p-JAK2, JAK2, p-STAT3, STAT3, IL-1β, TNF-α, and IL-6 in cell lysates from OGD/R-induced HBMECs treated with solvent DMSO, ADRB2 agonist Salbutamol, and ADRB2 antagonist ICI118551. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. Q - V Density quantification of ADRB2 ( Q ), p-JAK2 and JAK2 ( R ), p-STAT3 and STAT3 ( S ), IL-1β ( T ), TNF-α ( U ), IL-6 V . n = 6. W ELISA analysis of inflammatory cytokines IL-10 in the supernatants of OGD/R-induced HBMECs treated with solvent DMSO, ADRB2 agonist Salbutamol, and ADRB2 antagonist ICI118551. n = 3. Data were analyzed using one-way ANOVA, and post hoc Dunnett’s test to correct for P -values. All data are expressed as means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
Article Snippet: In addition, according to the literature, 100nM
Techniques: Quantitative RT-PCR, Biomarker Discovery, Plasmid Preparation, Over Expression, Western Blot, Knockdown, Transfection, Labeling, Enzyme-linked Immunosorbent Assay, Solvent
Journal: Journal of Neuroinflammation
Article Title: Curcumin reduces neuroinflammation and oxidative stress in a stroke model by epigenetically regulating ADRB2 methylation through JAK2/STAT3 and Nrf2/HO-1 pathways
doi: 10.1186/s12974-026-03729-y
Figure Lengend Snippet: ADRB2 gene is closely associated with oxidative stress in OGD/R-induced HBMECs. A Flowchart. B - D Expression levels of oxidative damage markers GSH ( B ), SOD ( C ), and MDA ( D ) in OGD/R-induced HBMECs treated with empty vector, ADRB2 knockdown siRNA, and ADRB2 overexpression plasmid. n = 3. E - G Expression levels of oxidative damage markers GSH ( E ), SOD ( F ), and MDA ( G ) in OGD/R-induced HBMECs treated with solvent DMSO, ADRB2 agonist Salbutamol, and ADRB2 antagonist ICI118551. n = 3. H Representative Western blot bands for Nrf2 and HO-1 in cell lysates from OGD/R-induced HBMECs treated with empty vector, ADRB2 knockdown siRNA, and ADRB2 overexpression plasmid. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. I - J Density quantification of Nrf2 ( I ) and HO-1 ( J ) proteins. n = 6. K Representative Western blot bands for Nrf2 and HO-1 in cell lysates from OGD/R-induced HBMECs treated with solvent DMSO, ADRB2 agonist Salbutamol, and ADRB2 antagonist ICI118551. The relative protein levels were normalized to β-actin from the same sample for Western blot analysis. L - M Density quantification of Nrf2 ( L ) and HO-1 ( M ) proteins. n = 6. N Representative fluorescence images of ROS in OGD/R-induced HBMECs treated with solvent DMSO, ADRB2 agonist Salbutamol, ADRB2 antagonist ICI118551, ADRB2 knockdown siRNA, and ADRB2 overexpression plasmid. White represents the bright-field image, and green indicates the fluorescence intensity of ROS. Scale bar, 100 μm. O Quantification of fluorescence ROS intensity. n = 3. Data were analyzed using one-way ANOVA, and post hoc Dunnett’s test to correct for P -values. All data are expressed as means ± SEM. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
Article Snippet: In addition, according to the literature, 100nM
Techniques: Expressing, Plasmid Preparation, Knockdown, Over Expression, Solvent, Western Blot, Fluorescence
Journal: Journal of Neuroinflammation
Article Title: Curcumin reduces neuroinflammation and oxidative stress in a stroke model by epigenetically regulating ADRB2 methylation through JAK2/STAT3 and Nrf2/HO-1 pathways
doi: 10.1186/s12974-026-03729-y
Figure Lengend Snippet: Validation of the correlation between ADRB2 and JAK2/STAT3 and Nrf2/HO-1 signaling in MCAO mice. A Flowchart. B Representative Western blot bands for ADRB2, p-JAK2, JAK2, p-STAT3, STAT3, Nrf2, and HO-1 in brain tissue lysates from the infarcted area of MCAO mice treated with DMSO, the ADRB2 agonist Salbutamol, or the ADRB2 antagonist ICI118551. The relative levels of each protein were normalized to β-actin from the same sample for Western blot analysis. (C-G) Quantification of ADRB2 ( C ), Nrf2 ( D ), HO-1 ( E ), p-JAK2 and JAK2 ( F ), p-STAT3 and STAT3 ( G ) protein densities. n = 3. H - J Expression levels of oxidative stress markers GSH ( H ), SOD ( I ), and MDA ( J ) in the infarcted area of MCAO mice treated with DMSO, Salbutamol, or ICI118551. n = 3. K Representative immunofluorescence images of the infarcted area in MCAO mice treated with DMSO, Salbutamol, or ICI118551, with red indicating fluorescence intensity of 4-HNE protein. Scale bar, 50 μm ( L ) Quantification of the average fluorescence intensity of 4-HNE. n = 3. M - P ELISA analysis of inflammatory cytokines IL-1β ( M ), IL-6 ( N ), TNF-α ( O ) and IL-10 ( P ) in brain tissue homogenates from the infarcted area of MCAO mice treated with DMSO, Salbutamol, or ICI118551. n = 3. All data are presented as means ± SEM, with statistical analysis performed using one-way ANOVA, and post hoc Dunnett’s test to correct for P -values. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
Article Snippet: In addition, according to the literature, 100nM
Techniques: Biomarker Discovery, Western Blot, Expressing, Immunofluorescence, Fluorescence, Enzyme-linked Immunosorbent Assay
Journal: Journal of Neuroinflammation
Article Title: Curcumin reduces neuroinflammation and oxidative stress in a stroke model by epigenetically regulating ADRB2 methylation through JAK2/STAT3 and Nrf2/HO-1 pathways
doi: 10.1186/s12974-026-03729-y
Figure Lengend Snippet: The targets of curcumin are ADRB2, JAK2/STAT3, and Nrf2/HO-1 axis. A Flowchart. B Representative Western blot bands for ADRB2, p-JAK2, JAK2, p-STAT3, STAT3, Nrf2, and HO-1 in brain tissue lysates from the infarcted area of MCAO mice treated with DMSO, Curcumin, and the ADRB2 antagonist ICI118551. The relative levels of each protein were normalized to β-actin from the same sample for Western blot analysis. C - G Quantification of ADRB2 ( C ), Nrf2 ( D ), HO-1 ( E ), p-JAK2 and JAK2 ( F ), p-STAT3 and STAT3 ( G ) protein densities. n = 6. H ELISA analysis of inflammatory cytokines IL-6 in brain tissue homogenates from the infarcted area of MCAO mice treated with DMSO, Curcumin, and the ADRB2 antagonist ICI118551. n = 3. I Expression levels of oxidative stress markers SOD in the infarcted area of MCAO mice treated with DMSO, Curcumin, and the ADRB2 antagonist ICI118551. n = 3. J Representative Western blot bands for ADRB2, Nrf2, and HO-1 in brain tissue lysates from the infarcted area of MCAO mice treated with DMSO, Salbutamol, and ML385. The relative levels of each protein were normalized to β-actin from the same sample for Western blot analysis. K - M Quantification of ADRB2 ( K ), Nrf2 ( L ), HO-1 ( M ) protein densities. n = 6. N Expression levels of oxidative stress markers SOD in the infarcted area of MCAO mice treated with DMSO, Salbutamol, and ML385. n = 3. O Representative Western blot bands for ADRB2, p-JAK2, JAK2, p-STAT3 and STAT3 in brain tissue lysates from the infarcted area of MCAO mice treated with DMSO, Salbutamol, and Coumermycin A1. The relative levels of each protein were normalized to β-actin from the same sample for Western blot analysis. P - R Quantification of ADRB2 ( P ), p-JAK2 and JAK2 ( Q ), p-STAT3 and STAT3 ( R ) protein densities. n = 6. S ELISA analysis of inflammatory cytokines IL-6 in brain tissue homogenates from the infarcted area of MCAO mice treated with DMSO, Salbutamol, and Coumermycin A1. n = 3. T Schematic diagram of various drug targets. All data are presented as means ± SEM, with statistical analysis performed using one-way ANOVA, and post hoc Tukey’s test to correct for P -values. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001
Article Snippet: In addition, according to the literature, 100nM
Techniques: Western Blot, Enzyme-linked Immunosorbent Assay, Expressing
Journal: Nature
Article Title: Tumour–brain crosstalk restrains cancer immunity via a sensory–sympathetic axis
doi: 10.1038/s41586-025-10028-8
Figure Lengend Snippet: a , Experimental setup (left), representative H&E-stained lung sections (middle) and tumour quantification (right) from Trpv1-cre; LSL-DTR mice that received VNG PBS injection (G1, n = 12), VNG DT injection (G2, n = 13) or VNG DT injection plus daily aerosolized salbutamol treatment (G3, n = 12). Lung tumour burden was assessed by tumour/tissue area (G1 versus G2: P = 0.0133; G2 versus G3: P = 0.0131) and total lung mass (G1 versus G2: P = 0.0101; G2 versus G3: P = 0.0005). Scale bars, 1 mm. b , Representative H&E-stained lung sections and tumour quantification from wild-type (WT, n = 7) and Adrb2 − / − mice ( n = 7). Lung tumour burden was assessed as tumour/tissue area ( P = 0.0398) and total lung mass ( P < 0.0001). Scale bars, 1 mm. c , d , Quantification of ARG1 + alveolar macrophages ( c ), IFNγ + TNF + CD8 T cells and TNF + CD4 T cells ( d ) in tumour-bearing lungs from wild-type ( n = 7) and Adrb2 − / − mice ( n = 5–6). c , P = 0.0004. d , CD8: P = 0.0037; CD4: P = 0.0213. e , Experimental setup (left), representative H&E-stained lung sections (middle) and tumour quantification (right) from irradiated Trpv1-cre; LSL-DTR mice that were reconstituted with wild-type or Adrb2 − / − bone marrow (BM) and injected with PBS or DT in the VNG. WT BM: n = 8 PBS (G1), n = 8 DT (G2); Adrb2 − / − BM: n = 10 PBS (G3), n = 10 DT (G4); pooled from 2 independent experiments. Scale bars, 1 mm. 5.1× and 1.3× denote fold change of tumour/tissue area between indicated groups. f , g , Quantification of ARG1 + alveolar macrophages ( f ), IFNγ + TNF + CD8 T cells and TNF + CD4 T cells ( g ) in tumour-bearing lungs from bone marrow chimeric mice described in e . h , i , Arg1 expression in cultured alveolar macrophages measured by quantitative PCR with reverse transcription (RT–qPCR). h , Wild-type alveolar macrophages were untreated or treated with 10 μM noradrenaline (NA) ( n = 4 per group, P < 0.0001). i , Wild-type or Adrb2 − / − alveolar macrophages were pretreated with 10 μM noradrenaline and then either left untreated ( n = 4 per group, P = 0.0001) or treated with TES ( n = 4 per group , P = 0.0073). Data are presented as fold change relative to untreated wild-type alveolar macrophages ( h , i ). Results shown are representative of at least two independent experiments. Data are expressed as mean ± s.e.m. Unpaired, two-tailed Student’s t -test ( b – d , h ) or one-way ANOVA with Tukey’s multiple comparisons ( a , e – g , i ). Exact P values for e – g are provided in the .
Article Snippet: For
Techniques: Staining, Injection, Irradiation, Expressing, Cell Culture, Real-time Polymerase Chain Reaction, Reverse Transcription, Quantitative RT-PCR, Two Tailed Test
Journal: Nature
Article Title: Tumour–brain crosstalk restrains cancer immunity via a sensory–sympathetic axis
doi: 10.1038/s41586-025-10028-8
Figure Lengend Snippet: a , Quantification of the number of KP tumour cells that were untreated (Ctrl) or treated with 10 μM norepinephrine (NE) for three days (triplicates for each condition). b , Experimental setup, representative H&E-stained lung sections, and quantification of lung tumour burden from Trpv1-cre; lsl-DTR ; Adrβ2 − / − mice injected with PBS (n = 9) or DT (n = 6) in the VNG. c , Quantification of ARG1 + AMs, IFNγ + TNFα + CD8 T cells, and TNFα + CD4 T cells in tumour-bearing lungs from the same mice as b. d-e , Quantification of ARG1 and surface MHC-II expression in AMs ( d ), and quantification of IFNγ + TNFα + CD8 T cells and TNFα + CD4 T cells ( e ) in tumour-bearing lungs from Trpv1-cre; lsl-DTR mice that received VNG PBS injection (n = 12, G1), VNG DT injection (n = 13, G2), or VNG DT injection plus daily aerosolized salbutamol treatment (n = 12, G3). d , ARG1: p = 0.1276 (G1 vs G2), p = 0.2619 (G2 vs G3); MHC-II: p < 0.0001 (G1 vs G2, G2 vs G3). e , CD8: p = 0.0797 (G1 vs G2), p = 0.0276 (G2 vs G3); CD4: p = 0.0456 (G1 vs G2), p = 0.0271 (G2 vs G3). f , Expressions of genes encoding adrenergic receptors in AMs sorted from healthy (n = 3) or tumour-bearing (n = 6) lungs as determined by bulk RNA-sequencing. g , Adrβ1 and Adrβ2 expression in AMs and CD8 T cells sorted from tumour-bearing lungs (n = 2) as determined by RT-qPCR. p = 0.0015. h , Tumour cell viability from in vitro T cell-killing assay. OT-I CD8 + T cells were co-cultured with OVA-expressing KP tumour cells in the presence or absence of norepinephrine (NE, 10 µM). Percentages of live tumour cells were determined by flow cytometry 24 h after co-culture. i , Experimental scheme, tumour quantification by total lung weight and representative H&E lung sections of WT or Adrβ2 − / − mice that were inoculated with KP tumour cells and intratracheally treated with PBS or clodronate liposomes. WT + PBS (n = 6, G1), Adrβ2 − / − + PBS (n = 7, G2), WT + clodronate (n = 6, G3), Adrβ2 − / − + clodronate (n = 8, G4). G1 vs G2: p = 0.0047, G3 vs G4: p = 0.5043, G1 vs G3: p = 0.0587, G2 vs G4: p = 0.9799. j , Quantification of IFNγ + TNFα + CD8 T cells and TNFα + CD4 T cells in tumour-bearing lungs from the same cohort in i . CD8: p = 0.0361 (G1 vs G2), p = 0.2254 (G3 vs G4), p = 0.0357 (G1 vs G3), p = 0.1563 (G2 vs G4); CD4: p = 0.0053 (G1 vs G2), p = 0.9741 (G3 vs G4), p = 0.1673 (G1 vs G3), p = 0.6366 (G2 vs G4). k , Quantification of IFNγ + TNFα + CD8 T cells and TNFα + CD4 T cells in tumour-bearing lungs from Trpv1-cre; lsl-DTR mice that were injected with PBS or DT in the VNG (n = 6 PBS, n = 5 DT), and intratracheally treated with clodronate liposome. l , Experimental setup of the mixed bone marrow chimera experiment in which irradiated Npy2r-ires-cre; lsl-DTR mice were reconstituted with Adrβ2 − / − and CD11c-cre; Pparg fl/fl bone marrow mixed at 1:1 ratio and injected with PBS or DT in the VNG (n = 12 PBS, n = 11 DT). CD11c-cre; Pparg fl/fl mice are deficient in AMs . m-o , Quantification of AM ARG1 and surface MHC-II expression ( m ), IFNγ + TNFα + CD8 T cells and TNFα + CD4 T cells ( n ) in the tumour-bearing lungs, and quantification of lung tumour burden ( o , n = 6 PBS, n = 7 DT) from the same chimeric cohort in l . p , Representative flow cytometry plots showing the gating strategy for exhausted CD8 T cells (Tex, defined as PD1 + TIM3 + TCF1 − CD44 + CD8 T cells). q-t , Quantification of Tex populations in tumour-bearing lungs from Npy2r-ires-cre; lsl-DTR mice injected with PBS or DT in the VNG ( q , n = 4 PBS, n = 6 DT), from Trpv1-cre; lsl-DTR mice that were injected with PBS or DT in the VNG ( r , n = 4 PBS, n = 5 DT), from WT ( s , n = 7) versus Adrβ2 − / − mice ( s , n = 6), and from vagal DT-injected Trpv1-cre; lsl-DTR mice that were either left untreated or treated daily with aerosolized salbutamol ( t , n = 13 DT, n = 12 DT+ salbutamol). Data are expressed as mean ± s.e.m. and representative of at least two independent experiments. Unpaired, two-tailed Student’s T-test ( a-c, g, k, m-o, q-t ) or one-way ANOVA with Tukey’s multiple comparisons ( d-e, h-j ) was performed.
Article Snippet: For
Techniques: Staining, Injection, Expressing, RNA Sequencing, Quantitative RT-PCR, In Vitro, Cell Culture, Flow Cytometry, Co-Culture Assay, Liposomes, Irradiation, Two Tailed Test
Journal: Journal of ethnopharmacology
Article Title: Evidence to support cultivated fruiting body of Ophiocordyceps sinensis (Ascomycota)'s role in relaxing airway smooth muscle.
doi: 10.1016/j.jep.2024.118727
Figure Lengend Snippet: Fig. 2. Effect of (a) OCS02® CWE at different time intervals (5- or 15-min) on tracheal rings (b) OCS02® CWE at 15-min interval on both tracheal (T) and bronchial (B) rings (c) Salbutamol against carbachol pre-contracted tracheal rings. Tissue responses are expressed as a percentage of carbachol-induced contraction and are shown as means ± SEM of 5–6 animals. Two-way ANOVA with Bonferroni correction analysis was conducted between vehicle control and treatment groups: (a & c) *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; (b) Trachea: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001; Bronchus: +p < 0.05, ++p < 0.01, ++++p < 0.0001.
Article Snippet: 4-Aminopyridine (Tocris, Bristol, UK), barium chloride (SigmaAldrich, Dorset, UK), carbachol (Nacalai Tesque, Kyoto, Japan), NGnitro-L-arginine methyl ester (Nacalai Tesque), S-(− )-propranolol hydrochloride (Santa Cruz, Dallas, TX, USA),
Techniques: Control
Journal: Communications Biology
Article Title: Bioluminescence resonance energy transfer-based biosensors allow monitoring of ligand- and transducer-mediated GPCR conformational changes
doi: 10.1038/s42003-018-0101-z
Figure Lengend Snippet: Effects of Gs and β-arrestin on conformational changes promoted by isoproterenol (ISO) and salbutamol (SALB). a Kinetics of the changes in BRET signal of the NY-β2AR conformational sensor upon ISO and SALB (100 μM) stimulation in HEK293T cells. Data are expressed as normalized ligand-promoted BRET changes; the maximal response of the biosensor in response to ISO being set as 100%. Although the ISO-promoted conformational change results in a decrease in BRET, the BRET changes are represented as positive responses. b Gαs-promoted change in the NY-β2AR conformational sensor BRET signal as a function of the amount of Gαs co-transfected. Data are expressed as the percentage of ISO response in the absence of over-expressed G protein. The response to ISO in the absence of over-expressed Gs is represented by the square symbol on the Y -axis. c , d Effect of co-transfection of Gs or β-arrestin (500 ng per 10 6 cells) on the kinetics of ISO-promoted and SALB-promoted conformational changes of the NY-β2AR sensor. Data are expressed as the percentage of ISO-promoted response in the absence of Gs and β-arrestin over-expression ( a ), the dotted line corresponding to the basal BRET signal observed in the presence of over-expressed Gs or β-arrestin in the absence of ligand. e , f Concentration–response curves of the ISO-stimulated NY-β2AR response in HEK293 cells lacking β-arrestin vs. their parental cells ( e ) or in HEK293 cells lacking Gs vs. their parental cells ( f ). g , h Basal BRET levels observed in the different cell lines. Statistical analysis was performed using an unpaired Student’s t test (* p value <0.05). Data are expressed as percentage of ISO response for the parental cell lines and represent the mean ± SEM of at least three independent experiments conducted in duplicates. i Schematic cartoon of ISO-induced vs. SALB-induced conformational changes
Article Snippet:
Techniques: Transfection, Cotransfection, Over Expression, Concentration Assay
Journal: Biosensors
Article Title: Rapid and Simple Buffer Exchange Using Cation-Exchange Chromatography to Improve Point-of-Care Detection of Pharmacological Agents.
doi: 10.3390/bios13060635
Figure Lengend Snippet: Figure 3. Comparison of LFA outputs versus albuterol concentration (ppb) for selected urine simu- lants. Aggregated LFA readout values from all urine simulants (n = 9) (A), from concentrated urine simulant (B), high salt only urine simulant, (C) and dilute urine simulant (D).
Article Snippet: LFAs to detect
Techniques: Comparison, Concentration Assay
Journal: Biosensors
Article Title: Rapid and Simple Buffer Exchange Using Cation-Exchange Chromatography to Improve Point-of-Care Detection of Pharmacological Agents.
doi: 10.3390/bios13060635
Figure Lengend Snippet: Figure 4. Comparison of LFA readout from two human saliva samples. LFAs with no processing return the same positive result if the samples contain 20 ppb albuterol (A) and 0 ppb albuterol (B). In comparison, processing using the method in this paper results in a clear signal when 20 ppb of albuterol is added to the sample (C) compared to when no albuterol is added (D) using either visual inspection (left) or an optical reader (right).
Article Snippet: LFAs to detect
Techniques: Comparison
Journal: International archives of allergy and immunology
Article Title: Regulation of T Helper Cell Type 2 Immune Response by Controlling Beta-2 Adrenergic Receptor in Dendritic Cells of Patients with Allergic Rhinitis.
doi: 10.1159/000531956
Figure Lengend Snippet: Fig. 4. Regulation of THP-1 derived DCs with the ADRB2 agonist/antagonist. Der p 1-matured DCs were treated with either Salbutamol (Sal, ADRB2 agonist) or ICI 118.551 (ICI, ADRB2 antagonist) for 24 h. a The mRNA level of ADRB2. **p value <0.01, n = 3. b The image of Western blot analysis. c Immunocytochemical staining of ADRB2 (green). Scale bar, 50 μm. d The graphical analysis of cAMP concentration. **p value <0.01.
Article Snippet: Immunofluorescence To determine the expression of ADRB2 in the THP-1 derivedDCs, DCs matured with/without Der p1, and Der p1 matured DCs with/ without
Techniques: Derivative Assay, Western Blot, Staining, Concentration Assay
Journal: International archives of allergy and immunology
Article Title: Regulation of T Helper Cell Type 2 Immune Response by Controlling Beta-2 Adrenergic Receptor in Dendritic Cells of Patients with Allergic Rhinitis.
doi: 10.1159/000531956
Figure Lengend Snippet: Fig. 5. Co-culture analysis for Th immune response between Der p 1-matured DCs and naïve CD4+ T cells. a Diagram of the in vitro co-culture system with Der p 1-matured DCs and naïve CD4+ T cells. b ELISA profile of cytokines in the co-culture medium. The medium was harvested from Der p 1-matured DCs treated with salbutamol (Sal) or not (control). *p value <0.05; **p value <0.01, n = 3.
Article Snippet: Immunofluorescence To determine the expression of ADRB2 in the THP-1 derivedDCs, DCs matured with/without Der p1, and Der p1 matured DCs with/ without
Techniques: Co-Culture Assay, In Vitro, Enzyme-linked Immunosorbent Assay, Control
Journal: International archives of allergy and immunology
Article Title: Regulation of T Helper Cell Type 2 Immune Response by Controlling Beta-2 Adrenergic Receptor in Dendritic Cells of Patients with Allergic Rhinitis.
doi: 10.1159/000531956
Figure Lengend Snippet: Fig. 6. In vivo effect of salbutamol administration in the AR mouse model. a Strategy for nasal administration of salbutamol for AR treatment in an OVA-1-induced AR mouse model. b Frequency of nasal rubbing and sneezing over a 15 min period. c Serum concentrations of total and OVA-1-specific IgE. d Histological evaluation of nasal mucosa. Arrows in the insert of Sirius red, eosinophils. Arrowheads in tryptase, mast cells. Scale bar, 500 μm. e Th cytokines were measured in nasal mucosa by quantitative real-time PCR. *p < 0.05 and **p < 0.01, n = 6.
Article Snippet: Immunofluorescence To determine the expression of ADRB2 in the THP-1 derivedDCs, DCs matured with/without Der p1, and Der p1 matured DCs with/ without
Techniques: In Vivo, Real-time Polymerase Chain Reaction