Background: LF 16-0687 Ms previously was reported to improve Neurological Severity Score (NSS) and decrease cerebral edema and prostaglandin E(2) (PGE(2)) release after closed head trauma (CHT) in rats. Here, we examined whether these beneficial effects of LF 16-0687 Ms are altered when CHT is accompanied by acute ethanol administration.
Methods: Six groups of rats (n = 8 per group) were examined during combination of the following experimental conditions: CHT versus sham operation, LF 16-0687 Ms 3 mg/kg subcutaneously versus saline, and ethanol 2 g/kg versus saline.
Results: After CHT, brain water content decreased and NSS improved with ethanol + LF 16-0687 Ms as compared with values after saline or ethanol. PGE(2) release decreased with ethanol (147 +/- 59 pg/mg tissue) but not with ethanol + LF 16-0687 Ms (286 +/- 194 pg/mg tissue).
Conclusion: Ethanol does not affect the improvement of NSS and the decrease of cerebral edema seen with LF 16-0687 Ms after CHT, but does reverse the ability of LF 16-0687 Ms to minimize the increase of PGE(2) release. In intoxicated patients, bradykinin antagonist therapy may improve post-CHT outcome without altering PGE(2) release.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1097/01.TA.0000079808.48268.EC | DOI Listing |
Alzheimers Dement
December 2024
Feil Family Brain and Mind Research Institute, Weill Cornell Medicine, New York, NY, USA.
Background: Multiple AD risk genes are implicated in lipid metabolism, and plasma and brain lipid levels are altered in AD. Astrocytes are enriched in key lipid-related factors and are likely contributors to altered lipid homeostasis in AD. We hypothesize that APP/Aβ-related pathology and neuroimmune factors modulate astrocytic gene transcription that promote maladaptive changes in lipid pathways, including aberrant astrocytic production and release of lipids that could affect Aβ pathology and neuronal deficits.
View Article and Find Full Text PDFBrain 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 PDFHeliyon
December 2024
Department of Surgery, University Hospital Regensburg, 93053, Regensburg, Germany.
Background: Routine liver function tests capture information about the metabolic and inflammatory condition of the liver, but we lack sensitive biomarkers of early hepatocyte stress. In humans, soluble CD46 (sCD46) levels in blood were recently identified as an accurate biomarker of hepatic steatosis. Here, we explore the diagnostic utility of sCD46 in other liver diseases.
View Article and Find Full Text PDFJ Clin Med
December 2024
Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), University of Barcelona, 08907 Barcelona, Spain.
In patients with aspirin-exacerbated respiratory disease (AERD), there is disparate regulation of prostaglandin E2 (PGE) and prostaglandin D (PGD). Both prostanoids are synthesised by cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2). However, while the basal synthesis of PGE tends to decrease, that of PGD increases in patients with AERD.
View Article and Find Full Text PDFBioorg Chem
December 2024
State Key Laboratory of Fine Chemicals, Department of Pharmaceutical Engineering, School of Chemical Engineering, Dalian University of Technology, 2 Linggong Road, Dalian 116024, PR China. Electronic address:
In this report, we disclose the design and synthesis of a series of 2-trifluoromethyl-2H- chromene ethers as novel COX-2 inhibitors with low ulcerogenicity. Among them, 6-fluoro-3-(4-methoxyphenyl)-2-(2-(thiophen-3-yl)ethoxy)-2-(trifluoromethyl)-2H-chromene (E25) significantly suppressed LPS-induced release of NO and PGE, expression of COX-2 and iNOS, and activation of NF-κB pathway. The inhibitory effect of E25 on human recombinant COX-2 (IC = 70.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!