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Crocetin is a natural carotenoid dicarboxylic acid derived from Crocus sativus. It has been utilized as natural biomedicine with healing effects. The immunoregulatory and anti-inflammatory properties may cause the biological activities of crocetin. Nevertheless, it is not still clear how this compound acts and causes an immune-modulatory impact on human lymphocytes. The effects of three concentrations (5, 10, and 20 μM) of crocetin or dexamethasone (0.1 mM) were assessed on gene expression and secretion of cytokines, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) level, and nitric oxide (NO) production in phytohaemagglutinin (PHA)-stimulated and non-stimulated lymphocytes. By incubation with PHA, gene expression and cytokine concentration comprising interferon (IFN)-γ, interleukin (IL)-17A, IL-10, and IL-4 were increased, along with NF-κB concentration and NO production (all, p < 0.001). In comparison with the controls, an alteration occurred in the T-helper (Th)2/Th1 and Th17/Treg balance in the stimulated lymphocyte toward a Th2 and Th17 response. In stimulated cells, crocetin and dexamethasone decreased pro-inflammatory significantly and increased anti-inflammatory cytokines and related gene expression, respectively. Moreover, Th17/Treg and Th1/Th2 balance was changed toward Treg and Th1 significantly reducing NF-κB and NO levels (p < 0.05 to p < 0.001). Promoting effects were represented by crocetin on T-cell subsets to Treg and Th1. Hence, it can have therapeutic value for treating predominant diseases of Th2 or Th17 cells., (© 2023 International Union of Biochemistry and Molecular Biology.)

Background: The oxygen required to meet metabolic needs of all tissues is delivered by the red blood cell (RBC), a small, flexible cell which, in mammals, is devoid of a nucleus and mitochondria. Despite its simple appearance, this cell has an important role in its own distribution, enabling the delivery of oxygen to precisely meet localized metabolic need. When red blood cells enter in hypoxic area, a signalling pathway is activated within the cell, resulting in the release of ATP in amounts adequate to activate purinergic receptors on vascular endothelium, which trigger secretion of nitric oxide and other factors resulting in vasodilatation., Objective: The present study investigates the effect of adenosine exposure on this molecular mechanism., Methods and Results: We report that RBC in the presence of adenosine in low oxygen conditions, ATP release increase after 24 h exposure. Adenosine induced-ATP release in deoxygenated red blood cell show data similar to that of RBC in high oxygen conditions: (1) RBC after band 3 modification by 4,4'- diisothio-cyanatostilbene- 2,2'-disulphonic acid; (2) CO-treated RBC. In the presence of Sphingosine kinase (SphK1) inhibitor, adenosine mediated effects on ATP release were abolished. Activity of adenylate cyclase increase following to adenosine exposure, on the contrary red cell phosphofructokinase is not modified within the RBC in the presence of adenosine., Conclusion: Our data support involvement of band 3/deoxyHb binding and adenylate cyclase in the pathway responsible for ATP release from RBC following exposure to adenosine.