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Image Search Results
Journal: International Journal of Molecular Sciences
Article Title: A Low-Sodium Diet Boosts Ang (1–7) Production and NO-cGMP Bioavailability to Reduce Edema and Enhance Survival in Experimental Heart Failure
doi: 10.3390/ijms22084035
Figure Lengend Snippet: Dietary sodium restriction activates classical and non-classical renin-angiotensin-aldosterone system (RAAS) in mice with DCM. ( A – D ) Effect of dietary sodium restriction on plasma levels of the classical RAAS: ( A ) renin activity (AU, arbitrary units), ( B ) angiotensin II (AngII), ( C ) aldosterone, and counter-regulatory RAAS: ( D ) angiotensin converting enzyme 2 (ACE2) and ( E ) angiotensin (1–7) (Ang (1–7)). Number of DCM mice n = 7–8 per group. WT control mice (dashed line, n = 5–8) at 17 weeks of age. Data are presented as mean ± SEM. **** p < 0.0001, *** p < 0.001, * p < 0.001 (DCM vs. WT); ++++ p < 0.0001, ++ p < 0.01, + p < 0.05 (DCM on NSD vs. DCM on LSD) by one-way ANOVA with Newman-Keuls multiple comparison test.
Article Snippet: Plasma levels of target proteins were measured by enzyme-linked immunosorbent assay (ELISA) as previously reported [ , , , , , , , ]: ANP (as N terminus-ANP), BNP (as C terminus-BNP) and angiotensin II (Phoenix Pharmaceuticals, Inc., Burlingame, CA, USA); cGMP (Enzo Life Science Inc., Farmingdale, NY, USA); corin (USCN Life Science Inc., Houston, TX, USA);
Techniques: Activity Assay
Journal: International Journal of Molecular Sciences
Article Title: A Low-Sodium Diet Boosts Ang (1–7) Production and NO-cGMP Bioavailability to Reduce Edema and Enhance Survival in Experimental Heart Failure
doi: 10.3390/ijms22084035
Figure Lengend Snippet: Low-sodium diet increases the nitric oxide (NO) plasma levels in mice with DCM. ( A ) Total nitrite (NO 2 − ) and nitrate (NO 3 − ) plasma levels (NOx = NO 2 − + NO 3 − ). ( B ) 3-nitrotyrosine levels, (3-NT). DCM mice on NSD n = 8, on LSD n = 7–9 per group. ( C – E ) Suppression of plasma levels of ( C ) total nitrite/nitrate, ( D ) cGMP and, ( E ) Ang (1–7) by short-term L-NAME (N-nitro-L-arginine methyl ester) tail vein infusion. Number of DCM mice L-NAME(−) n = 8–9 per group; L-NAME(+) n = 5 per group. WT control mice (dashed line, n = 8). Data are presented as mean ± SEM, **** p < 0.0001, * p < 0.05 (DCM vs. WT), and ++++ p < 0.0001, +++ p < 0.001, ++ p < 0.01 (DCM on LSD vs. DCM on NSD). Data were analyzed by one-way ANOVA with Newman–Keuls multiple comparison test ( A , B ), by unpaired t -test ( C , E ) or by Mann–Whitney test ( D ).
Article Snippet: Plasma levels of target proteins were measured by enzyme-linked immunosorbent assay (ELISA) as previously reported [ , , , , , , , ]: ANP (as N terminus-ANP), BNP (as C terminus-BNP) and angiotensin II (Phoenix Pharmaceuticals, Inc., Burlingame, CA, USA); cGMP (Enzo Life Science Inc., Farmingdale, NY, USA); corin (USCN Life Science Inc., Houston, TX, USA);
Techniques: MANN-WHITNEY
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 1 Effects of Ang-(1–7) on ATG5 protein expression in IL-13-treated BEAS-2B and HBSMC cells. A BEAS-2B and HBSMC cells were treated with different dose (5, 10, 20, 40 µM) of Ang-(1–7) for 24 h. Cell viability was measured via a CCK-8 kit. BEAS-2B and HBSMC cells were treated with 10 ng/mL human IL-13 for 24 h, then treated with different dose (5, 10, 20 µM) of Ang-(1–7) for 24 h. Expression of ATG5 protein in BEAS-2B cells (B) and HBSMC cells (C) was measured by western blotting. *p < 0.05, **p < 0.01. ns: no significance
Article Snippet: The Ang-(
Techniques: Expressing, CCK-8 Assay, Western Blot
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 2 Ang-(1–7) treatment suppressed the expression of Beclin-1 protein and secretions of IL-25 and IL-33 in the IL-13-treated BEAS-2B cells. BEAS-2B cells were transfected with control siRNA or ATG5 siRNA, and then treated with IL-13 for 24 h. The IL-13-treated cells were treated with 20 µM Ang-(1–7) for 24 h, and the PBS treatment was as a control treatment. A Cell viability in different groups was measured using a CCK-8 kit. B Expression of Beclin-1 protein was measured using Western blotting. C Secretion of IL-25 and IL-33 was measured using ELISA kits. ns: no significance. *p < 0.05, **p < 0.01
Article Snippet: The Ang-(
Techniques: Expressing, Transfection, Control, CCK-8 Assay, Western Blot, Enzyme-linked Immunosorbent Assay
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 3 Ang-(1–7) treatment suppressed the expression of Beclin-1, TGF-β1 and α-SMA protein in the IL-13-treated HBSMC cells. HBSMC cells were transfected with control siRNA or ATG5 siRNA, and then treated with IL-13 for 24 h. The IL-13-treated cells were treated with 20 µM Ang-(1–7) for 24 h, and the PBS treatment was as a control treatment. A Cell viability was measured using a CCK-8 kit. B Expression of Beclin-1 protein was measured using Western blotting. C Expression of TGF-β1 and α-SMA protein was measured using Western blotting. ns: no significance. *p < 0.05, **p < 0.01
Article Snippet: The Ang-(
Techniques: Expressing, Transfection, Control, CCK-8 Assay, Western Blot
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 4 Ang-(1–7) suppressed the results of ATG5 overexpression in IL-13-induced BEAS-2B cells. The BEAS-2B cells were transfected with ATG5 cDNA or vector control, and treated with IL-13 for 24 h. The ATG5 cDNA-transfected or vector control-transfected cells were treated with 20 µM Ang-(1–7) treatment. A Expression of Beclin-1 protein was measured using Western blotting. B Secretion of IL-25 and IL-33 was measured using ELISA kits. **p < 0.01
Article Snippet: The Ang-(
Techniques: Over Expression, Transfection, Plasmid Preparation, Control, Expressing, Western Blot, Enzyme-linked Immunosorbent Assay
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 5 Ang-(1–7) suppressed the results of ATG5 overexpression in IL-13-induced HBSMC cells. The HBSMC cells were transfected with ATG5 cDNA or vector control, and treated with IL-13 for 24 h. The ATG5 cDNA-transfected or vector control-treated cells were treated with 20 µM Ang-(1–7) treatment. A Expression of Beclin-1, TGF-β1 and α-SMA protein was measured using Western blotting. B Relative expression of Beclin-1 protein was normalized by GAPDH. C Relative expression of TGF-β1 protein was normalized by GAPDH. D Relative expression of α-SMA protein was normalized by GAPDH. *p < 0.05, **p < 0.01
Article Snippet: The Ang-(
Techniques: Over Expression, Transfection, Plasmid Preparation, Control, Expressing, Western Blot
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 6 Ang-(1–7) treatment or ATG5 knockout suppressed airway inflammation in OVA-challenged mice. A The diagram of animal treatments. An allergic asthma model was induced by OVA in WT mice and ATG5.−/− mice. The OVA-induced WT mice were treated with 30 µg/kg/d Ang-(1–7) for 10 days after sensitization at day 8. B Airway resistance to methacholine were measured. C Levels of IL-4, IL-5 and IL-33 in BALFs were measured using ELISA kits. D Observation of pathological changes by H&E staining. Area of inflammatory infiltration in airway was analyzed using ImageJ software. **p < 0.01
Article Snippet: The Ang-(
Techniques: Knock-Out, Enzyme-linked Immunosorbent Assay, Staining, Software
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 7 Ang-(1–7) treatment or ATG5 knockout suppressed airway remodeling in by OVA-challenged mice. Expression of α-SMA (A) and TGF-β1 (B) in airway was analyzed by immunohistochemical analysis. Expression of results was analyzed by ImageJ software. *p < 0.05, **p < 0.01
Article Snippet: The Ang-(
Techniques: Knock-Out, Expressing, Immunohistochemical staining, Software
Journal: BMC pulmonary medicine
Article Title: Angiotensin-(1-7) suppresses airway inflammation and airway remodeling via inhibiting ATG5 in allergic asthma.
doi: 10.1186/s12890-023-02719-7
Figure Lengend Snippet: Fig. 8 Ang-(1–7) treatment or ATG5 knockout suppressed airway autophagy in OVA-challenged mice. A Expression of LC3B in airway was evaluated by immunohistochemical analysis. B Expression of Beclin-1 in airway was evaluated by western blotting. *p < 0.05, **p < 0.01
Article Snippet: The Ang-(
Techniques: Knock-Out, Expressing, Immunohistochemical staining, Western Blot