eNOS Blocking Peptide
- Known as:
- eNOS Blocking Peptide
- Catalog number:
- 33r-10759
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Fitzgerald industries international
- Gene target:
- eNOS Blocking Peptide
Ask about this productRelated genes to: eNOS Blocking Peptide
- Gene:
- NOS3 NIH gene
- Name:
- nitric oxide synthase 3
- Previous symbol:
- -
- Synonyms:
- ECNOS, eNOS
- Chromosome:
- 7q36.1
- Locus Type:
- gene with protein product
- Date approved:
- 1993-08-23
- Date modifiied:
- 2016-10-05
Related products to: eNOS Blocking Peptide
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Publication date: 2026/09/28
Zhou TaoZhang XinyuYang JinghongWang Juan - : Periodontitis is a chronic inflammatory disease characterized by dysregulated host immune responses that drive connective tissue destruction and alveolar bone loss. Human gingival fibroblasts (HGFs) are central regulators of periodontal inflammation through their production of cytokines, chemokines, matrix-remodeling enzymes, and other inflammatory mediators. Although cannabinoid receptor 2 (CB2) activation has demonstrated anti-inflammatory properties, its coordinated effects on multiple inflammatory pathways in gingival fibroblasts remain poorly understood. This study investigated the transcriptomic effects of the selective CB2 agonist HU-308 on IL-1β-induced inflammatory responses in HGFs. : Primary HGFs were divided into untreated controls, IL-1β-stimulated cells (10 ng/mL), and IL-1β-stimulated cells treated with HU-308 (10 μM). Twenty-four hours after stimulation, transcriptome-wide expression profiling was performed using Affymetrix Human Clariom S microarrays, followed by targeted analysis of selected inflammation-related transcriptional domains. Selected transcripts were evaluated within predefined biological domains including cytokines, chemokines, extracellular matrix-associated genes, NO/cGMP-related genes, transporter-associated genes, and GPCR-related transcripts. Gene expression was analyzed using one-way ANOVA with Tukey's post hoc test. : IL-1β induced a coordinated inflammatory transcriptional program characterized by increased expression of pro-inflammatory cytokines, chemokines, matrix metalloproteinases, glucose transporter genes, and multiple GPCR-related transcripts, while suppressing collagen-associated genes, NOS3, GPR4, and GPR78. HU-308 broadly attenuated these inflammatory responses by reducing the expression of cytokines, chemokines, matrix metalloproteinases, and several GPCR-related genes while restoring collagen-associated transcripts, nitric oxide signaling components, anti-inflammatory mediators, and selected glucose transporters toward basal levels. Schematic multidimensional visualizations were used to illustrate relative expression patterns among selected transcripts within each functional domain; these visualizations do not represent statistically derived gene networks or molecular interactions. : Pharmacological modulation of CB2 by HU-308 exerts broad immunomodulatory effects in IL-1β-stimulated human gingival fibroblasts by coordinately regulating multiple transcriptional networks involved in periodontal inflammation. These findings demonstrate that HU-308 treatment is associated with coordinated modulation of inflammatory, extracellular matrix, nitric oxide, metabolic, and GPCR-associated transcriptional pathways in IL-1β-stimulated HGFs. The results support the hypothesis that CB2 signaling may participate in the broader regulation of these interconnected responses; however, receptor-specific studies using CB2 antagonism or CNR2 knockdown are required to establish causality. - Source: PubMed
Publication date: 2026/09/06
Arain UswaDedman KeeganCooper MatthewAshfaq ObaedAit-Aissa KarimaMunkhsaikhan UndralHoque Apu EhsanulSahyoun Amal MajedDabbous MustafaKassan ModarAbidi Ammaar H - (1) Background: Endothelial nitric oxide synthase (eNOS/NOS3), the main source of vascular nitric oxide (NO), generates superoxide instead of NO when oxidative stress uncouples it. Circulating eNOS in the early puerperium is uncharacterised. (2) Methods:In a single-centre cross-sectional study (Timișoara, Romania, July 2022), 40 mother-newborn dyads were evaluated. Maternal serum eNOS protein was quantified by ELISA on postpartum day 1, alongside pre-delivery laboratory data and Edinburgh Postnatal Depression Scale (EPDS) screening. Analyses (Spearman correlation, linear regression, prevalence odds) were unadjusted for multiplicity; only correlations of |ρ| ≥ 0.44 were detectable at 80% power. (3) Results:Median serum eNOS was 8.997 ng/mL (interquartile range 4.091-27.985). eNOS correlated inversely with total and LDL cholesterol (ρ = -0.368, = 0.027; ρ = -0.412, = 0.013) and positively with erythrocyte count (ρ = 0.326, = 0.046). The association with maternal age was similar in magnitude but non-significant (ρ = -0.303, = 0.061). Multivariable models were not significant, and eNOS was unrelated to EPDS score (ρ = 0.111, = 0.512). (4) Conclusions:Lower circulating eNOS protein, not enzyme activity, accompanied a less favourable lipid profile, but not depressive symptoms. These single-centre Romanian findings are hypothesis-generating and should not be generalised. - Source: PubMed
Publication date: 2026/09/16
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Publication date: 2026/09/24
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