Journal: Circulation

Article Title: Aldosterone Enhances Ischemia-Induced Neovascularization Through Angiotensin II–Dependent Pathway

doi: 10.1161/01.cir.0000127112.36796.9b

Figure Lengend Snippet: Figure 1. Representative photomicro- graphs and quantitative evaluation of microangiography (A), capillary density (B; capillary appears in white, and arrows indicate representative examples of fibronectin-positive capillaries), and foot perfusion (C). D, Representative pho- tomicrographs of Western blot and quantitative evaluation of VEGF protein content. Values are meanSEM; n7. *P0.05 vs control mice; #P0.05 vs aldosterone-treated mice; †P0.05 vs nonischemic control. C indicates untreated animals; A, aldosterone-treated mice; AS, aldosterone and spironolac- tone–treated mice; AV, aldosterone and valsartan–treated mice; Aa-VEGF, aldo- sterone and neutralizing VEGF–treated mice; Mb, membrane stained with pon- ceau red; N. Isch., nonischemic; Isch., ischemic; Cont, control; and Aldo, aldosterone.

Article Snippet: C57Bl/6 mice (aged 10 weeks; Iffa Creddo, Lyon, France) were anesthetized by isoflurane inhalation, and unilateral hindlimb ischemia was induced by ligature (tied for complete occlusion) on the right femoral artery, as previously described).4,6 Mice were then randomly assigned to one of the following groups (n 7): (1) control group: vehicle (1% ethanol in drinking water); (2) mice receiving the mineralocorticoid receptor blocker spironolactone (spironolactone dissolved in ethanol at 25 mg/mL and added to drinking water; mice then received 20 mg/kg per day; Sigma); (3) mice treated with the AT1 receptor blocker valsartan (drinking water, 20 mg/kg per day; Sigma); (4) aldosterone (4.5 g/d by osmotic minipumps implanted subcutaneously in the back of the mice; model 2004, Alza Corp); (5) aldosterone plus spironolactone; (6) aldosterone plus valsartan; and (7) aldosterone plus a-VEGF neutralizing antibody (10 g IP twice per week; R&D Systems).

Techniques: Western Blot, Control, Membrane, Staining

Journal: Journal of Inflammation Research

Article Title: Valsartan Mitigates the Progression of Methotrexate-Induced Acute Kidney Injury in Rats via the Attenuation of Renal Inflammation and Oxidative Stress

doi: 10.2147/JIR.S456610

Figure Lengend Snippet: Semiquantitative Histopathological Scoring Analysis of Changes in the Kidneys of Rats

Article Snippet: Methotrexate and Valsartan were purchased from TargetMol, Massachusetts, United States (MolPort-003-665-521 and MolPort-003-666-608 respectively) and dissolved in DMSO (dimethyl sulfoxide; Millipore, Molsheim, France).

Techniques: Control

Journal: Free radical biology & medicine

Article Title: Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina.

doi: 10.1016/j.freeradbiomed.2014.03.020

Figure Lengend Snippet: Fig. 1. Suppression of light-induced visual function impairment by ARBs. Analysis of full-field ERG after light exposure. (A) Representative wave forms of the ERG from an individual mouse treated with one of the ARBs, valsartan, in each dosage group in response to one flash. (B, C) Amplitudes of the a-wave and b-wave were decreased 6 days after light exposure, and these changes were suppressed by treatment with ARBs in a dose-dependent manner. (D, E) No differences were observed in the a-wave or b-wave implicit times. ERG, electroretinogram; ARBs, angiotensin II type 1 receptor blockers; C, control; LE, light exposure; val, valsartan; los, losartan; can, candesartan. n ¼ 6 in each group. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. **P o 0.01, *P o 0.05.

Article Snippet: Valsartan (LKT Laboratories, St. Paul, MN, USA) and candesartan (Sigma–Aldrich, St. Louis, MO, USA) were solubilized in dimethyl sulfoxide (Sigma–Aldrich), followed by dilution with phosphatebuffered saline (PBS).

Techniques: Control

Journal: Free radical biology & medicine

Article Title: Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina.

doi: 10.1016/j.freeradbiomed.2014.03.020

Figure Lengend Snippet: Fig. 2. Suppression of light-induced histological changes in the retina by valsartan. (A) H-E staining of retinal sections 6 days after light exposure. (B) The ONL thickness and (C) the OS length in the retina of light-exposed mice were reduced compared with those of untreated control mice. This reduction was significantly attenuated by valsartan administration (5 mg/kg). (D, E) TUNEL assay performed 2 days after light exposure. TUNEL-positive cells (red) appeared in the ONL after light exposure. These apoptotic cells were significantly reduced by valsartan administration (5 mg/kg). Hoechst staining of the control was shown as a guide for the retinal layers. GCL, ganglion cell layer; INL, inner nuclear layer; ONL, outer nuclear layer; OS, outer segment; ■, control mice with no light exposure; ●, light-exposed mice treated with vehicle; ○, light-exposed mice treated with valsartan. n ¼ 6 in each group. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. **P o 0.01, *P o 0.05.

Article Snippet: Valsartan (LKT Laboratories, St. Paul, MN, USA) and candesartan (Sigma–Aldrich, St. Louis, MO, USA) were solubilized in dimethyl sulfoxide (Sigma–Aldrich), followed by dilution with phosphatebuffered saline (PBS).

Techniques: Staining, Control, TUNEL Assay

Journal: Free radical biology & medicine

Article Title: Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina.

doi: 10.1016/j.freeradbiomed.2014.03.020

Figure Lengend Snippet: Fig. 3. Inhibition of light-induced ROS accumulation by treatment with valsartan. Detection of ROS by DHE staining 1 h after light exposure. (A, B) The fluorescence intensity of DHE in the ONL measured by ImageJ was increased after light exposure. The light-induced increase in ROS levels was prevented by treatment with valsartan (5 mg/kg). ONL, outer nuclear layer. n ¼ 6 in each group. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. **P o 0.01, *P o 0.05.

Article Snippet: Valsartan (LKT Laboratories, St. Paul, MN, USA) and candesartan (Sigma–Aldrich, St. Louis, MO, USA) were solubilized in dimethyl sulfoxide (Sigma–Aldrich), followed by dilution with phosphatebuffered saline (PBS).

Techniques: Inhibition, Staining

Journal: Free radical biology & medicine

Article Title: Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina.

doi: 10.1016/j.freeradbiomed.2014.03.020

Figure Lengend Snippet: Fig. 5. Attenuation of light-induced molecular changes by treatment with either valsartan or NAC. (A, B) The mRNA level of c-fos measured by quantitative real-time RT-PCR, 1 h after light exposure, was significantly attenuated in the retinas of light-exposed mice treated with either (A) valsartan or (B) NAC, compared with vehicle-treated mice. (C, D) The increase in the fasl mRNA level 6 h after light exposure was significantly attenuated in the retinas of light-exposed mice treated with either (C) valsartan or (D) NAC, compared with vehicle-treated mice. Valsartan was administered at 5 mg/kg and NAC was at 250 or 500 mg/kg. The NAC-induced suppression was dose-dependent (B, D). NAC, N-acetyl-L-cysteine. n ¼ 6. Statistical analysis was performed using one-way ANOVA with Tukey’s post hoc test. **P o 0.01, *P o 0.05.

Article Snippet: Valsartan (LKT Laboratories, St. Paul, MN, USA) and candesartan (Sigma–Aldrich, St. Louis, MO, USA) were solubilized in dimethyl sulfoxide (Sigma–Aldrich), followed by dilution with phosphatebuffered saline (PBS).

Techniques: Quantitative RT-PCR