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Vector Laboratories animal free blocking solution
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Millipore pafr blocker cv-3988
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AstraZeneca ltd candesartan
A) Schematic diagram of experiment 1 study design and endpoints. GK rats were subjected to 3 h MCAO then treated with IV 1 mg/kg of the <t>AT1R</t> blocker, <t>candesartan,</t> at reperfusion. Animals were sacrificed at 24 h. B) Continuous blood pressure monitoring by telemetry showed an average basal blood pressure of 109 ± 2 mm Hg. MCAO increased blood pressure abruptly to 147 ± 4 mm Hg. Treatment with a single dose of candesartan reduced blood pressure to an average of 120 ± 3 mm Hg during the first 24 h, versus 135 ± 3 mm Hg for saline-treated animals. X-axis represents the time of day in hours. Animals were stroked at the same time (9:00) every day to control for any diurnal variation in blood pressure. Light is turned off in animal facility from 18:00 to 6:00 as represented by black line on X-axis. MAP: mean arterial pressure. C) Neurobehavioral testing was conducted using the three-point Bederson score. Animals scored 3 and 2.7 on average in the saline and candesartan-treated groups, respectively. D) Assessment of hemoglobin content in brain tissue homogenate was conducted using a specific ELISA kit. Hemoglobin content decreased from 80.9 ± 25 to 64 ± 19 μg/mg protein with treatment. The change, however, did not reach significance. E, F) Analysis of NY and 4-HNE levels in both saline and candesartan-treated groups was conducted using slot blot. No change was observed in the oxidative or nitrative stress markers with treatment at 24 h. G) Quantification of cleaved caspase-3 at the same time point showed a trend towards decreasing the cell death marker (18% decrease) with the treatment, that did not reach significance (n = 6 and 8 in saline and candesartan-treated groups, respectively), ns: no statistical significance, * = p < 0.05 vs corresponding contralesional side.
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Image Search Results


A) Schematic diagram of experiment 1 study design and endpoints. GK rats were subjected to 3 h MCAO then treated with IV 1 mg/kg of the AT1R blocker, candesartan, at reperfusion. Animals were sacrificed at 24 h. B) Continuous blood pressure monitoring by telemetry showed an average basal blood pressure of 109 ± 2 mm Hg. MCAO increased blood pressure abruptly to 147 ± 4 mm Hg. Treatment with a single dose of candesartan reduced blood pressure to an average of 120 ± 3 mm Hg during the first 24 h, versus 135 ± 3 mm Hg for saline-treated animals. X-axis represents the time of day in hours. Animals were stroked at the same time (9:00) every day to control for any diurnal variation in blood pressure. Light is turned off in animal facility from 18:00 to 6:00 as represented by black line on X-axis. MAP: mean arterial pressure. C) Neurobehavioral testing was conducted using the three-point Bederson score. Animals scored 3 and 2.7 on average in the saline and candesartan-treated groups, respectively. D) Assessment of hemoglobin content in brain tissue homogenate was conducted using a specific ELISA kit. Hemoglobin content decreased from 80.9 ± 25 to 64 ± 19 μg/mg protein with treatment. The change, however, did not reach significance. E, F) Analysis of NY and 4-HNE levels in both saline and candesartan-treated groups was conducted using slot blot. No change was observed in the oxidative or nitrative stress markers with treatment at 24 h. G) Quantification of cleaved caspase-3 at the same time point showed a trend towards decreasing the cell death marker (18% decrease) with the treatment, that did not reach significance (n = 6 and 8 in saline and candesartan-treated groups, respectively), ns: no statistical significance, * = p < 0.05 vs corresponding contralesional side.

Journal: Neurochemistry international

Article Title: Contralesional angiotensin type 2 receptor activation contributes to recovery in experimental stroke

doi: 10.1016/j.neuint.2022.105375

Figure Lengend Snippet: A) Schematic diagram of experiment 1 study design and endpoints. GK rats were subjected to 3 h MCAO then treated with IV 1 mg/kg of the AT1R blocker, candesartan, at reperfusion. Animals were sacrificed at 24 h. B) Continuous blood pressure monitoring by telemetry showed an average basal blood pressure of 109 ± 2 mm Hg. MCAO increased blood pressure abruptly to 147 ± 4 mm Hg. Treatment with a single dose of candesartan reduced blood pressure to an average of 120 ± 3 mm Hg during the first 24 h, versus 135 ± 3 mm Hg for saline-treated animals. X-axis represents the time of day in hours. Animals were stroked at the same time (9:00) every day to control for any diurnal variation in blood pressure. Light is turned off in animal facility from 18:00 to 6:00 as represented by black line on X-axis. MAP: mean arterial pressure. C) Neurobehavioral testing was conducted using the three-point Bederson score. Animals scored 3 and 2.7 on average in the saline and candesartan-treated groups, respectively. D) Assessment of hemoglobin content in brain tissue homogenate was conducted using a specific ELISA kit. Hemoglobin content decreased from 80.9 ± 25 to 64 ± 19 μg/mg protein with treatment. The change, however, did not reach significance. E, F) Analysis of NY and 4-HNE levels in both saline and candesartan-treated groups was conducted using slot blot. No change was observed in the oxidative or nitrative stress markers with treatment at 24 h. G) Quantification of cleaved caspase-3 at the same time point showed a trend towards decreasing the cell death marker (18% decrease) with the treatment, that did not reach significance (n = 6 and 8 in saline and candesartan-treated groups, respectively), ns: no statistical significance, * = p < 0.05 vs corresponding contralesional side.

Article Snippet: Animals were randomized to receive 1 mg/kg of candesartan (AT1R blocker, a gift from AstraZeneca) or saline at reperfusion via tail vein injection ( ).

Techniques: Saline, Control, Enzyme-linked Immunosorbent Assay, Dot Blot, Marker

A, B) Western blotting showed no difference in baseline angiotensin receptors expression between sham Wistars and GK rats. C, D) Quantification of AT1R expression showed a significant upregulation in the ischemic hemispheres of Wistars and GKs at 24 h. Candesartan decreased the receptor expression in Wistars with no change with treatment in GKs. E) Quantification of AT2R expression showed a significant upregulation in contralateral hemisphere of Wistars. Candesartan treatment further increased the receptor expression. F) GK rats showed a significant decrease in AT2R expression that was not rescued by candesartan treatment at 24 h, n = 3–4, 6, 6 for sham, saline and candesartan groups, respectively, * = p < 0.05. G) Preincubation with C21 enhanced relaxation to Ach in control animals (AUC: vehicle 146.7 + 3.9 vs C21 pretreatment 229.6 + 11.6) which was abolished by the blockade of AT2R (176.9 + 25.5, p = 0.007). Similarly, C21 improved sensitivity in control animals (EC50: vehicle 110.5 + 32 vs C21 pretreatment 11.9 + 2) which was abolished in the presence of PD129319 (93.8 + 31, p = 0.04), *C21 vs other groups. H) Basilar artery relaxation was impaired in diabetic GK rats as compared to controls and C21 had no effect.

Journal: Neurochemistry international

Article Title: Contralesional angiotensin type 2 receptor activation contributes to recovery in experimental stroke

doi: 10.1016/j.neuint.2022.105375

Figure Lengend Snippet: A, B) Western blotting showed no difference in baseline angiotensin receptors expression between sham Wistars and GK rats. C, D) Quantification of AT1R expression showed a significant upregulation in the ischemic hemispheres of Wistars and GKs at 24 h. Candesartan decreased the receptor expression in Wistars with no change with treatment in GKs. E) Quantification of AT2R expression showed a significant upregulation in contralateral hemisphere of Wistars. Candesartan treatment further increased the receptor expression. F) GK rats showed a significant decrease in AT2R expression that was not rescued by candesartan treatment at 24 h, n = 3–4, 6, 6 for sham, saline and candesartan groups, respectively, * = p < 0.05. G) Preincubation with C21 enhanced relaxation to Ach in control animals (AUC: vehicle 146.7 + 3.9 vs C21 pretreatment 229.6 + 11.6) which was abolished by the blockade of AT2R (176.9 + 25.5, p = 0.007). Similarly, C21 improved sensitivity in control animals (EC50: vehicle 110.5 + 32 vs C21 pretreatment 11.9 + 2) which was abolished in the presence of PD129319 (93.8 + 31, p = 0.04), *C21 vs other groups. H) Basilar artery relaxation was impaired in diabetic GK rats as compared to controls and C21 had no effect.

Article Snippet: Animals were randomized to receive 1 mg/kg of candesartan (AT1R blocker, a gift from AstraZeneca) or saline at reperfusion via tail vein injection ( ).

Techniques: Western Blot, Expressing, Saline, Control