The binding of antagonists of histamine receptors H1 (promethazine) and H2 (ranitidine) by peripheral blood lymphocytes from pollinotics was determined before and after the course of immunotherapy. We found that lymphocytes from atopic subjects showed significant decrease in the binding of H2 receptor antagonist as compared to control subjects. Specific immunotherapy induced statistically significant increase in H2 receptor antagonist binding, which correlated with the improvement of clinical symptoms.
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Front Immunol
January 2025
Department of Bioengineering, College of Engineering, University of Toledo, Toledo, OH, United States.
Resolution of inflammation is essential for normal tissue healing and regeneration, with macrophages playing a key role in regulating this process through phenotypic changes from a pro-inflammatory to an anti-inflammatory state. Pharmacological and mechanical (mechanotherapy) techniques can be employed to polarize macrophages toward an anti-inflammatory phenotype, thereby diminishing inflammation. One clinically relevant pharmacological approach is the inhibition of Transient Receptor Potential Vanilloid 4 (TRPV4).
View Article and Find Full Text PDFOncol Lett
March 2025
College of Pharmacy, Korea University, Sejong 30019, Republic of Korea.
Cancer stem cells (CSCs) contribute to the resistance of intractable prostate cancer, and dopamine receptor (DR)D2 antagonists exhibit anticancer activity against prostate cancer and CSCs. Human prostate cancer PC-3 cells were used to generate CSC-like cells, serving as a surrogate system to identify the specific DR subtype the inhibition of which significantly affects prostate-derived CSCs. Additionally, the present study aimed to determine the downstream signaling molecules of this DR subtype that exert more profound effects compared with other DR subtypes.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Department of Cardiovascular Center, First Affiliated Hospital of Huzhou University, Huzhou, China.
The emergence of targeted anti-tumor drugs has significantly prolonged the lifespan and improved the prognosis of cancer patients. Among these drugs, vascular endothelial growth factor (VEGF) inhibitors, particularly novel small molecule tyrosine kinase inhibitors (TKIs), are extensively employed as VEGF inhibitors; however, they are also associated with a higher incidence of complications, with hypertension being the most prevalent cardiovascular toxic side effect. Currently, it is widely accepted that TKIs-induced hypertension involves multiple mechanisms including dysregulation of the endothelin (ET) axis, reduced bioavailability of nitric oxide (NO), imbalance in NO-ROS equilibrium system, vascular rarefaction, and activation of epithelial sodium calcium channels; nevertheless, excessive activation of ET system appears to be predominantly responsible for this condition.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Institute for Personalized Oncology, Center for Digital Biodesign and Personalized Healthcare, First Moscow State Medical University of the Ministry of Health of Russia (Sechenov University), Moscow, Russia.
Background: The natural killer (NK) activity of peripheral blood mononuclear cells (PBMCs) is a crucial defense against the onset and spread of cancer. Studies have shown that patients with reduced NK activity are more susceptible to cancer, and NK activity tends to decrease due to cancer-induced immune suppression. Enhancing the natural cytotoxicity of PBMCs remains a significant task in cancer research.
View Article and Find Full Text PDFIran J Basic Med Sci
January 2025
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Objectives: Traumatic brain injury (TBI) is a significant cause of mortality and disability worldwide. TBI has been associated with factors such as oxidative stress, neuroinflammation, and apoptosis, which are believed to be mediated by the N-methyl-D-aspartate (NMDA)-type glutamate receptor. Two NMDA receptor antagonists, ketamine and memantine, have shown potential in mitigating the pathophysiological effects of TBI.
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