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PGE and HCN2 ion channels are critical mediators of pain initiated by angiotensin II.
Brain Behav Immun
December 2024
Wolfson Sensory, Pain and Regeneration Centre, King's College London, Guy's Campus, London Bridge, London SE1 1UL, UK. Electronic address:
Angiotensin II is well known to have an important influence on blood pressure, mediated via the angiotensin II type 1 receptor (AT1R), and more recent studies have shown that angiotensin II may play an important additional role in eliciting pain via a distinct action at the angiotensin II type 2 receptor (AT2R). Signalling pathways that link activation of AT2R to a sensation of pain are, however, incompletely understood. Here we use rodent inflammatory pain models to confirm that selective activation of AT2R triggers aversive responses, and that these are abolished by either antagonism or genetic deletion of AT2R.
View Article and Find Full Text PDFCelecoxib paradoxically induces COX-2 expression and astrocyte activation through the ERK/JNK/AP-1 signaling pathway in the cerebral cortex of rats.
Neurochem Int
December 2024
Master and PhD Programs in Pharmacology and Toxicology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970; Department of Pharmacology, School of Medicine, Tzu Chi University, Hualien, Taiwan 970. Electronic address:
Previous studies have shown that celecoxib or NSAID may paradoxically induce cyclooxygenase-2 (COX-2) expression and trigger inflammation-like responses in airway smooth muscle cells and renal mesangial cells. Despite the extensive research on celecoxib, its atypical biological effect on the induction of COX-2 in astroglial cells within the central nervous system (CNS) remains unexplored. In the present study, we investigated the impact of celecoxib on COX-2 and Glial Fibrillary Acidic Protein (GFAP) expression and explored the mechanisms underlying celecoxib-regulated COX-2 expression in cortical astrocytes of rats.
View Article and Find Full Text PDFInducing phospholipase A2 and cyclooxygenase-2 expression and prostaglandins' production of human dental pulp cells by activation of NOD receptor and its downstream signaling.
Int J Biol Macromol
December 2024
School of Dentistry, National Taiwan University Medical College, Taipei, Taiwan; Department of Dentistry, National Taiwan University Hospital, Taipei, Taiwan; School of Dentistry, College of Dental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Dentistry, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan. Electronic address:
Dental caries with invasion and infection by microorganisms may induce pulpitis and intolerable pain. L-Ala-γ-D-Glu-mDAP (TriDAP) is a DAP-comprising muramyl tripeptide and a peptidoglycan degradation product found in gram-negative pulpal pathogens. TriDAP activates nucleotide-binding oligomerization domain1/2 (NOD1/NOD2) and induces tissue inflammatory responses.
View Article and Find Full Text PDFSQSTM1 upregulation-induced iron overload triggers endothelial ferroptosis in nicotine-exacerbated atherosclerosis.
Life Sci
December 2024
Department of Anesthesiology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University & Fujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fujian Provincial Key Laboratory of Critical Medicine, Fujian Provincial Co-constructed Laboratory of "Belt and Road", Fuzhou, Fujian 350001, China. Electronic address:
Aims: Nicotine-exacerbated atherosclerosis significantly increases global mortality. Endothelial cells, which line the interior of blood vessels, are crucial for maintaining vascular function. How nicotine is involved in vascular remodeling in atherosclerosis via modulating endothelial dysfunction remains unknown.
View Article and Find Full Text PDFProstanoid signaling in retinal cells elicits inflammatory responses relevant to early-stage diabetic retinopathy.
J Neuroinflammation
December 2024
Department of Pharmacology, Vanderbilt University, Nashville, TN, USA.
Inflammation is a critical driver of the early stages of diabetic retinopathy (DR) and offers an opportunity for therapeutic intervention before irreversible damage and vision loss associated with later stages of DR ensue. Nonsteroidal anti-inflammatory drugs (NSAIDs) have shown mixed efficacy in slowing early DR progression, notably including severe adverse side effects likely due to their nonselective inhibition of all downstream signaling intermediates. In this study, we investigated the role of prostanoids, the downstream signaling lipids whose production is inhibited by NSAIDs, in promoting inflammation relevant to early-stage DR in two human retinal cell types: Müller glia and retinal microvascular endothelial cells.
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