rabbit anti human kinin b1r primary antibody  (Bioss)

Journal: Basic & Clinical Pharmacology & Toxicology

Article Title: Antagonism of Kinin Receptors B1 and B2 Attenuates Folic Acid‐Induced Tubulointerstitial Fibrosis in Mice

doi: 10.1111/bcpt.70189

Figure Lengend Snippet: Kinin B1R antagonism worsens acute kidney injury induced by folic acid. Kidney function was assessed 48 h after folic acid administration by measuring serum creatinine (A) and urea (B) levels. Kidney injury markers KIM‐1 (C) and NGAL (D) were quantified by quantitative real‐time PCR. Tubular injury scores were determined from haematoxylin and eosin–stained kidney sections (E–F). M1 and M2 macrophage markers were analysed by real‐time PCR (G–H) across three experimental groups: Vehicle, FA (folic acid–treated) and FA + R715 (folic acid treated with the B₁ receptor antagonist R715). Continuous data (creatinine, urea and gene expression) are presented as mean ± SEM and were analysed using one‐way ANOVA followed by Tukey's post hoc test. Ordinal data (tubular injury scores) are presented as medians with ranges and were analysed using the Kruskal–Wallis test followed by Dunn's post hoc test. Scale bars = 50 μm. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. n = 5–6 animals per group.

Article Snippet: TaqMan probe assays included Bdkb1r (Mm00432059_s1), Bdkb2r (Mm00437788_s1) and Gapdh (Mm99999915_g1).

Techniques: Real-time Polymerase Chain Reaction, Staining, Gene Expression

Journal: Basic & Clinical Pharmacology & Toxicology

Article Title: Antagonism of Kinin Receptors B1 and B2 Attenuates Folic Acid‐Induced Tubulointerstitial Fibrosis in Mice

doi: 10.1111/bcpt.70189

Figure Lengend Snippet: Kinin B1R antagonism prevents the progression of chronic kidney disease induced by folic acid. Renal function was evaluated 28 days after folic acid administration by measuring serum creatinine (A), urea (B) and proteinuria (C) levels. Kidney injury markers KIM‐1 (D), NGAL (E) and TNF‐ α (F) were quantified by quantitative real‐time PCR. Renal fibrosis was assessed using picrosirius red‐stained kidney sections (G–H), and fibrotic marker expression was evaluated in renal tissue by real‐time PCR (I) across three experimental groups: Vehicle, FA (folic acid–treated) and FA + R715 (folic acid treated with the B₁ receptor antagonist R715). Continuous data (creatinine, urea, proteinuria and gene expression) are presented as mean ± SEM and were analysed using one‐way ANOVA followed by Tukey's post hoc test. Ordinal data (fibrosis scores) are presented as medians with ranges and were analysed using the Kruskal–Wallis test followed by Dunn's post hoc test. Scale bars = 100 μm. * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001. n = 4–6 animals per group.

Article Snippet: TaqMan probe assays included Bdkb1r (Mm00432059_s1), Bdkb2r (Mm00437788_s1) and Gapdh (Mm99999915_g1).

Techniques: Real-time Polymerase Chain Reaction, Staining, Marker, Expressing, Gene Expression

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: WIN55,212‐2 increases blood pressure in a B1R‐dependent manner. (a) Experimental schematic showing acute intravenous injection of WIN55,212‐2 (400 μg/kg) via the jugular vein, followed by blood pressure measurement and tissue collection. (b) Mean arterial pressure (MAP) response to WIN55,212‐2 in wild‐type (WT) and B1 receptor knockout (B1RKO) mice. WIN55,212‐2 significantly increased MAP in WT but not in B1RKO mice, suggesting a B1R‐dependent mechanism. Data are presented as mean ± SD. Repeated measures 2‐way ANOVA, n = 3–6 mice/group.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Injection, Knock-Out

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: Brain and cardiac expression of B1R, CB1R, and oxidative stress following WIN55,212‐2 administration. Representative images and quantification of B1R (a), CB1R (b), and oxidative stress (DHE, c) expression in the paraventricular nucleus (PVN) of the hypothalamus. Images and corresponding expressions of B1R (d), CB1R (e), and oxidative stress (DHE, f) in heart tissue. WIN55,212‐2 increased CB1R expression and oxidative stress in WT but not B1RKO mice in both brain and heart. Data are presented as mean ± SD. n = 3–6 mice/group; 2‐way ANOVA with Tukey's multiple comparisons test.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Expressing

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: Effects of WIN55,212‐2 on oxidative stress and mitochondrial function in H9c2 cardiomyocytes and human cardiac fibroblasts. Quantification of DHE (a), B1R (b), CB1R (c), mitochondrial superoxide (MitoSOX, d), and mitochondrial membrane potential (TMRE, e) in H9c2 cardiomyocytes following WIN55,212‐2 treatment. WIN55,212‐2 in H9c2 cells increased oxidative stress, B1R, and CB1R expression, and decreased mitochondrial membrane potential. Corresponding quantification of DHE (f), B1R (g), CB1R (h), MitoSOX (i), and TMRE (j) in human cardiac fibroblasts. Unlike H9c2 cells, WIN55,212‐2 did not significantly alter TMRE in HCFs, despite increasing oxidative stress and receptor expression. Data are presented as mean ± SD. n = 3–6 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Membrane, Expressing

Journal: Physiological Reports

Article Title: Kinin B1 receptor mediates acute cardiovascular and neural responses following cannabinoid receptor 1 activation in conscious male mice

doi: 10.14814/phy2.70579

Figure Lengend Snippet: WIN55,212‐2‐induced effects in primary neurons are mediated in part by B1R. Quantification of CB1R (a), DHE (b), and B1R (c) expression following WIN55,212‐2 with or without B1R antagonist pretreatment. WIN55,212‐2 increased CB1R, B1R and oxidative stress, and was attenuated by pharmacological inhibition of B1R. Mitochondrial superoxide (MitoSOX, d) and membrane potential (TMRE, e) showed impaired mitochondrial function with WIN55,212‐2, partially rescued by B1R antagonism. Data are presented as mean ± SD. n = 5–8 independent cultures/group: One‐way ANOVA followed by Tukey's multiple comparisons.

Article Snippet: Samples were incubated at 4°C overnight in B1R (1:250, ABR‐011, Alomone Labs), CB1R (1:200, custom), or MAP2 (1:500, NBP3‐05552, Novus Biologicals).

Techniques: Expressing, Inhibition, Membrane