antibody against enos  (Novus Biologicals)

Journal: World Journal of Gastroenterology

Article Title: Evaluation of a 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet-induced mouse model in a comparative experimental study of portal hypertension

doi: 10.3748/wjg.v32.i9.114207

Figure Lengend Snippet: The 3,5-diethoxycarbonyl-1,4-dihydrocollidine diet mouse model (4 weeks) exhibited significant liver sinusoidal endothelial cell dysfunction. A: Scanning electron microscopy (SEM) of liver sinusoids in normal chow diet (NCD) and 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) diet mouse models; B: Statistical analysis of fenestrae number and porosity; C: SEM of liver sinusoids in sham and bile duct ligation (BDL) mouse models; D: Statistical analysis of fenestrae number and porosity; E: SEM of liver sinusoids in oil, 8-week carbon tetrachloride (CCl 4 ), and 12-week CCl 4 mouse models; F: Statistical analysis of fenestrae number and porosity; G and H: Protein expression and quantitative analysis of total endothelial nitric oxide synthase (eNOS) and phosphorylated eNOS (p-eNOS) in NCD and DDC diet mouse livers; I and J: Protein expression and quantitative analysis of total eNOS and p-eNOS in sham and BDL mouse livers; K-M: Protein expression and quantitative analysis of total eNOS and p-eNOS in oil, 8-week CCl 4 , and 12-week CCl 4 mouse livers; N: Immunohistochemistry staining for lymphatic vessel endothelial hyaluronan receptor 1 (LyVE-1), cluster of differentiation (CD) 34, and von Willebrand factor (vWF) in livers of the three model groups; O-W: Quantitative analysis of positive staining areas for LyVE-1, CD34, and vWF. Sample sizes ( n ): 8:8 (normal chow diet vs 3,5-diethoxycarbonyl-1,4-dihydrocollidine), 8:7 (sham vs bile duct ligation), and 8:7:8 (oil vs 8-week carbon tetrachloride vs 12-week carbon tetrachloride). a P < 0.05. b P < 0.01. c P < 0.001. NS: No significant; NCD: Normal chow diet; DDC: 3,5-diethoxycarbonyl-1,4-dihydrocollidine; BDL: Bile duct ligation; CCl 4 : Carbon tetrachloride; eNOS: Endothelial nitric oxide synthase; p-eNOS: Phosphorylated endothelial nitric oxide synthase; GAPDH: Glyceraldehyde-3-phosphate dehydrogenase; LyVE-1: Lymphatic vessel endothelial hyaluronan receptor 1; vWF: Von Willebrand factor; CD: Cluster of differentiation.

Article Snippet: Membranes were probed with primary antibodies against endothelial nitric oxide synthase (eNOS) (1:1000, Cell Signaling), phosphorylated eNOS (p-eNOS) (1:1000, Affinity), and glyceraldehyde 3-phosphate dehydrogenase (1:5000, Proteintech).

Techniques: Electron Microscopy, Ligation, Expressing, Immunohistochemistry, Staining

Journal: ACS Omega

Article Title: PI3K/AKT/eNOS Modulation and Angiotensin II Suppression by Dryopteris crassirhizoma Rhizome Extract: Computational and Experimental Evidence

doi: 10.1021/acsomega.5c07735

Figure Lengend Snippet: Endothelium-dependent vasorelaxant effect of DCW via the PI3K/AKT/eNOS pathway. (A) Vasorelaxant effect of DCW on endothelium-intact (Endo+) aortic rings and corresponding isotonic tension traces. (B) Vasorelaxant effect and isotonic changes in endothelium-denuded (Endo−) aortic rings following DCW treatment. (C) Dose–response curves and isotonic traces showing the effect of PI3K inhibitors (LY294002 and Wortmannin) on DCW-induced vasorelaxation. (D) Effects of pretreatment with L-NAME (NOS inhibitor), ODQ (sGC inhibitor), MB (cGMP inhibitor), and indomethacin (COX inhibitor) on DCW-induced vasorelaxation. (E) Effects of AKT inhibition with MK-2206 (pan-AKT kinase inhibitor) attenuated DCW-induced vasorelaxation. (F) Western blot analysis of eNOS, p-AKT, AKT, and β-actin in aortic rings treated with DCW or amlodipine (AM), with densitometry presented as p-AKT/AKT and eNOS/β-actin (fold of control, CON). Panels A–E are shown as mean ± SEM ( n = 4); Panel F (Western blot densitometry) is shown as mean ± SD ( n = 3). * p < 0.05, ** p < 0.01, *** p < 0.001 vs control. AM, amlodipine; DCW, Dryopteris crassirhizoma Rhizome water extract; L-NAME, L-N G -nitro arginine methyl ester; sGC, soluble guanylyl cyclase; ODQ, 1H-[1,2,4]­oxadiazole­[4,3- a ]­quinoxalin-1-one; cGMP, cyclic guanosine monophosphate; MB, methylene blue; COX, cyclooxygenase; INDO, indomethacin; and PE, phenylephrine.

Article Snippet: Primary antibodies against p-eNOS (Ser1177, Cell Signaling Technology #9570), eNOS (#9572), p-AKT (Ser473, #4060), AKT (pan, #4691), and β-actin (#4970) were obtained from Cell Signaling Technology (Danvers, MA, USA).

Techniques: Inhibition, Western Blot, Control