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The Eagle Bioscience’s Glutathione Total Assay was utilized in a recent publication that explored how Diosmin mitigates dexamethasone-induced osteoporosis in vivo. Check out the full text and abstract below!

Abstract

Secondary osteoporosis is commonly caused by long-term intake of glucocorticoids(GCs), such as dexamethasone (DEX). Diosmin, a natural substance with potent antioxidant and anti-inflammatory properties, is clinically used for treating some vascular disorders. The current work targeted exploring the protective properties of diosmin to counteract DEX-induced osteoporosis in vivo. Rats were administered DEX (7 mg/kg) once weekly for 5 weeks, and in the second week, vehicle or diosmin (50 or 100 mg/kg/day) for the next four weeks. Femur bone tissues were collected and processed for histological and biochemical examinations. The study findings showed that diosmin alleviated the histological bone impairments caused by DEX. In addition, diosmin upregulated the expression of Runt-related transcription factor 2 (Runx2) and phosphorylated protein kinase B (p-AKT) and the mRNA transcripts of Wingless (Wnt) and osteocalcin. Furthermore, diosmin counteracted the rise in the mRNA levels of receptor activator of nuclear factor-kB ligand (RANKL) and the reduction in osteoprotegerin (OPG), both were induced by DEX. Diosmin restored the oxidant/antioxidant equilibrium and exerted significant antiapoptotic activity. The aforementioned effects were more pronounced at the dose level of 100 mg/kg. Collectively, diosmin has proven to protect rats against DEX-induced osteoporosis by augmenting osteoblast and bone development while hindering osteoclast and bone resorption. Our findings could be used as a stand for recommending supplementation of diosmin for patients chronically using GCs.

Arafa, El-Shaimaa A., et al. “Diosmin Mitigates Dexamethasone-Induced Osteoporosis in Vivo: Role of Runx2, Rankl/OPG, and Oxidative Stress.” Biomedicine & Pharmacotherapy, vol. 161, 2023, p. 114461.

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The Eagle Bioscience’s Lipid Peroxidase Assay was utilized in a recent publication that explored how hypercholesterolemia aggravates in-stent restenosis in rabbits. Check out the full text and abstract below!

Abstract

Competing Interest Statement

The authors have declared no competing interest.

Fishbein, Ilia, et al. Hypercholesterolemia Aggravates In-Stent Restenosis in Rabbits: A Mitigating Effect of Stent Surface Modification with CD47-Derived Peptide, 2023.

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The Eagle Bioscience’s Cortisol ELISA Assay was highlighted in a recent publication that focused on suppressive action of nesfatin-1 and nesfatin-1-like peptide on cortisol synthesis. Check out the full text and abstract below!

Abstract

Nasri, Atefeh, et al. Suppressive Action of Nesfatin-1 and Nesfatin-1-like Peptide on Cortisol Synthesis in Adrenal Cortex Cells, 2023, https://doi.org/10.21203/rs.3.rs-2595841/v1.

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The Eagle Bioscience’s easYmer HLA-A*03:01 MHC Tetramers Kit was utilized in a recent publication that explored T cells specific for α-myosin drive immunotherapy-related myocarditis. Check out the full text and abstract below.

Abstract

Immune-related adverse events, particularly severe toxicities such as myocarditis, are major challenges to the utility of immune checkpoint inhibitors (ICIs) in anticancer therapy¹. The pathogenesis of ICI-associated myocarditis (ICI-MC) is poorly understood. Pdcd1^–/–Ctla4^+/– mice recapitulate clinicopathological features of ICI-MC, including myocardial T cell infiltration². Here, using single-cell RNA and T cell receptor (TCR) sequencing of cardiac immune infiltrates from Pdcd1^–/–Ctla4^+/– mice, we identify clonal effector CD8⁺ T cells as the dominant cell population. Treatment with anti-CD8-depleting, but not anti-CD4-depleting, antibodies improved the survival of Pdcd1^–/–Ctla4^+/– mice. Adoptive transfer of immune cells from mice with myocarditis induced fatal myocarditis in recipients, which required CD8⁺ T cells. The cardiac-specific protein α-myosin, which is absent from the thymus^3,4, was identified as the cognate antigen source for three major histocompatibility complex class I-restricted TCRs derived from mice with fulminant myocarditis. Peripheral blood T cells from three patients with ICI-MC were expanded by α-myosin peptides. Moreover, these α-myosin-expanded T cells shared TCR clonotypes with diseased heart and skeletal muscle, which indicates that α-myosin may be a clinically important autoantigen in ICI-MC. These studies underscore the crucial role for cytotoxic CD8⁺ T cells, identify a candidate autoantigen in ICI-MC and yield new insights into the pathogenesis of ICI toxicity.

Axelrod, M.L., Meijers, W.C., Screever, E.M. et al. T cells specific for α-myosin drive immunotherapy-related myocarditis. Nature 611, 818–826 (2022).

If you have any questions about the easYmer HLA-A*03:01 MHC Tetramers Kit or our other offerings, please contact us here.

The Eagle Bioscience’s Serotonin ELISA Assay was utilized in a recent publication that explored how gut enterochromaffin cells drive visceral pain and anxiety. Check out the full text and abstract below.

Abstract

Gastrointestinal (GI) discomfort is a hallmark of most gut disorders and represents an important component of chronic visceral pain. For the growing population afflicted by irritable bowel syndrome, GI hypersensitivity and pain persist long after tissue injury has resolved². Irritable bowel syndrome also exhibits a strong sex bias, afflicting women three times more than men. Here, we focus on enterochromaffin (EC) cells, which are rare excitable, serotonergic neuroendocrine cells in the gut epithelium. EC cells detect and transduce noxious stimuli to nearby mucosal nerve endings but involvement of this signaling pathway in visceral pain and attendant sex differences has not been assessed. By enhancing or suppressing EC cell function in vivo, we show that these cells are sufficient to elicit hypersensitivity to gut distension and necessary for the sensitizing actions of isovalerate, a bacterial short-chain fatty acid associated with GI inflammation. Remarkably, prolonged EC cell activation produced persistent visceral hypersensitivity, even in the absence of an instigating inflammatory episode. Furthermore, perturbing EC cell activity promoted anxiety-like behaviors which normalized after blockade of serotonergic signaling. Sex differences were noted across a range of paradigms, indicating that the EC cell–mucosal afferent circuit is tonically engaged in females. Our findings validate a critical role for EC cell–mucosal afferent signaling in acute and persistent GI pain, in addition to highlighting genetic models for studying visceral hypersensitivity and the sex bias of gut pain.

Bayrer, James R., et al. “Gut Enterochromaffin Cells Drive Visceral Pain and Anxiety.” Nature, vol. 616, no. 7955, 2023, pp. 137–142., https://doi.org/10.1038/s41586-023-05829-8.

If you have any questions about our Serotonin ELISA Assay or our other offerings, please contact us here.

The Eagle Bioscience’s Pepsinogen I ELISA Kit was highlighted in a recent publication that focused on the discrimination between precancerous gastric lesions and gastritis. Check out the full text and abstract below.

Abstract

Murphy, John, et al. “Discrimination between Precancerous Gastric Lesions and Gastritis Using a Gastric Cancer Risk Stratification Model.” Asian Pacific Journal of Cancer Prevention, vol. 24, no. 3, 2023, pp. 935–943., https://doi.org/10.31557/apjcp.2023.24.3.935.

If you have any questions about our Pepsinogen I ELISA Kit or our other offerings, please contact us here.

The Eagle Bioscience’s Calprotectin ELISA Assay was utilized in a recent publication that focused on the gut microbiota of people with asthma. Check out the full text and abstract below.

Abstract

Wilson, Naomi G., et al. “The Gut Microbiota of People with Asthma Influences Lung Inflammation in Gnotobiotic Mice.” IScience, vol. 26, no. 2, 2023, p. 105991.

If you have any questions about our Calprotectin ELISA Assay or our other offerings, please contact us here.

The Eagle Bioscience’s Noradrenaline (Norepinephrine) Sensitive ELISA was utilized in a recent publication that focused on epinephrine versus vasopressin in an ovine model of perinatal cardiac arrest. Check out the full text and abstract below.

Abstract

Background: Current neonatal resuscitation guidelines recommend the use of epinephrine for bradycardia/arrest not responding to ventilation and chest compressions. Vasopressin is a systemic vasoconstrictor and is more effective than epinephrine in postnatal piglets with cardiac arrest. There are no studies comparing vasopressin with epinephrine in newly born animal models with cardiac arrest induced by umbilical cord occlusion.

Objective: To compare the effect of epinephrine and vasopressin on the incidence and time to return of spontaneous circulation (ROSC), hemodynamics, plasma drug levels, and vasoreactivity in perinatal cardiac arrest.

Design/Methods: Twenty-seven term fetal lambs in cardiac arrest induced by cord occlusion were instrumented and resuscitated following randomization to epinephrine or vasopressin through a low umbilical venous catheter.

Results: Eight lambs achieved ROSC prior to medication. Epinephrine achieved ROSC in 7/10 lambs by 8 ± 2 min. Vasopressin achieved ROSC in 3/9 lambs by 13 ± 6 min. Plasma vasopressin levels in nonresponders were much lower than responders after the first dose. Vasopressin caused in vivo increased pulmonary blood flow and in vitro coronary vasoconstriction.

Conclusions: Vasopressin resulted in lower incidence and longer time to ROSC compared to epinephrine in a perinatal model of cardiac arrest supporting the current recommendations for exclusive use of epinephrine in neonatal resuscitation.

Rawat, Munmun, et al. “Masked Randomized Trial of Epinephrine versus Vasopressin in an Ovine Model of Perinatal Cardiac Arrest.” Children, vol. 10, no. 2, 2023, p. 349.

If you have any questions about the Noradrenaline (Norepinephrine) Sensitive ELISA or our other offerings, please contact us here.