Alpinia katsumadai is known to suppress thromboxane A2 (TXA2) receptor agonist-induced scratching in mice. The specific components of A. katsumadai responsible for these biological effects, however, are not known. In the present study, we investigated whether cardamonin (CDN), one of major principles of A. katsumadai, has suppressive effects on TXA2-induced scratching in mice. Scratching induced by U46619 (the TXA2 receptor agonist) at a dose of 10nmol/site was shown to be suppressed by CDN (0.1nmol-0.5nmol/site). Suppression of the U46619-induced scratching response by CDN was found to be unrelated to competition with the ligand at the TXA2 receptor, since CDN did not suppress [(3)H] SQ29548 (the TXA2 receptor antagonist) binding to TXA2 receptor. TXA2 receptor expression in A549, HaCaT, and SH-SY5Y cell lines was examined and determined to be significant in the A549 and SH-SY5Y cell lines. Further, binding of high molecular G protein Gh/transglutaminase-2 (Gh/Tgase-2) to TXA2 receptor was confirmed in the A549 and SH-SY5Y cells by co-immunoprecipitation. CDN suppressed the binding of TXA2 receptor with Gh/Tgase-2, which also acts as a G protein involved in TXA2 signaling. These results suggested that CDN suppresses TXA2 receptor agonist-induced scratching by suppressing TXA2 signaling, specifically via blocking of the binding of Gh/Tgase-2 to TXA2 receptor.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.pbb.2014.09.011 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
[Determination of three metabolites of thromboxane A and 8-iso-prostaglandin F in urine by ultra performance liquid chromatography-tandem mass spectrometry].
Se Pu
February 2025
Shanghai-MOST Key Laboratory of Health and Disease Genomics, NHC Key Lab of Reproduction Regulation, Shanghai Institute for Biomedical and Pharmaceutical Technologies, Shanghai 200237, China.
Thromboxane A (TXA), a prothrombotic factor that induces platelet aggregation and thrombosis, acts as a vasoconstrictor by activating TXA receptors (TP receptors). TXA is extremely unstable and metabolizes into three major metabolites: 2,3-dinor thromboxane B (2,3-dinor-TXB), 11-dehydro TXB(11-dh-TXB), and 11-dehydro-2,3-dinor TXB(11-dh-2,3-dinor-TXB). 8-Iso-prostaglandin F(8-iso-PGF), a prostaglandin-like compound widely considered the best biomarker of oxidative stress, can also activate TP receptors.
View Article and Find Full Text PDF[Effect of Dendrobii Officinalis Caulis water extract on hyperviscosity rats based on TLR4/NF-κB/ICAM-1 signaling pathway].
Zhongguo Zhong Yao Za Zhi
October 2024
School of Pharmaceutical Sciences, Zhejiang Chinese Medical University Hangzhou 310053, China.
This study aims to reveal the effect and mechanism of Dendrobii Officinalis Caulis water extract on the rat model of hyperviscosity induced by a high-sugar, high-salt, and high-fat diet. Thirty-six male SD rats were randomized into normal, model, Compound Danshen Tablets(0.5 g·kg~(-1)), and low-, medium-, and high-dose(0.
View Article and Find Full Text PDFSeratrodast inhibits ferroptosis by suppressing lipid peroxidation.
Cell Death Dis
November 2024
Research Unit Signaling and Translation, Helmholtz Zentrum München, Neuherberg, Germany.
Ferroptosis is a regulated and non-apoptotic form of cell death mediated by iron-dependent peroxidation of polyunsaturated fatty acyl tails in phospholipids. Research of the past years has shed light on the occurrence of ferroptosis in organ injury and degenerative diseases of the brain, kidney, heart, and other tissues. Hence, ferroptosis inhibition may prove therapeutically beneficial to treat distinct diseases.
View Article and Find Full Text PDFDeletion of TP signaling in macrophages delays liver repair following APAP-induced liver injury by reducing accumulation of reparative macrophage and production of HGF.
Inflamm Regen
October 2024
Department of Pharmacology, Kitasato University School of Medicine, Sagamihara, Japan.
Article Synopsis
- Acetaminophen (APAP) can cause significant liver damage, and macrophages are critical for healing this injury; however, the role of thromboxane A (TXA) and its receptor in this process is not well understood.
- Research involved both TP knockout mice and wild-type mice treated with APAP to examine liver inflammation and repair.
- Results showed that lack of TP signaling in macrophages worsened liver injury and delayed repair, highlighting the importance of TP in supporting macrophage function and promoting recovery from APAP-induced liver damage.
NADPH oxidase 1/4 dual inhibitor setanaxib suppresses platelet activation and thrombus formation.
Life Sci
November 2024
College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea; Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Republic of Korea. Electronic address:
Aims: The production of reactive oxygen species (ROS) by NADPH oxidase (NOX) is able to induce platelet activation, making NOX a promising target for antiplatelet therapy. In this study, we examined the effects of setanaxib, a dual NOX1/4 inhibitor, on human platelet function and ROS-related signaling pathways.
Materials And Methods: In collagen-stimulated human platelets, aggregometry, assessment of ROS and Ca, immunoblotting, ELISA, flow cytometry, platelet adhesion assay, and assessment of mouse arterial thrombosis were performed in this study.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!