rhamnetin has been researched along with Inflammation* in 2 studies
2 other study(ies) available for rhamnetin and Inflammation
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Rhamnetin ameliorates macrophage-mediated inflammation and pro-atherosclerosis pathways in apolipoprotein E-deficient mice.
The present study was performed to examine the protective effects of rhamnetin against the development of atherosclerosis and its effects on the regulation of several pathways. The anti-atherosclerosis effect of rhamnetin was examined in cells stimulated with oxidized low-density lipoprotein (ox-LDL) by estimating the percentages of foam cell formation and apoptotic cells and determining the expression of specific proteins. As an in vivo model of atherosclerosis, apolipoprotein E-deficient (ApoE-/-) mice were treated with intragastric rhamnetin at 100 or 200 mg/kg for 8 weeks. The levels of inflammatory cytokines and oxidative stress parameters were determined in the aortic tissue of rhamnetin-treated ApoE-/- mice. The effects of rhamnetin on the Toll-like receptor 4 (TLR-4) pathway were assessed by quantitative reverse transcription polymerase chain reaction. The results of this study suggest that rhamnetin reduces the percentages of foam cells and apoptotic cells and the expression of CD36 and TLR-4 protein in ox-LDL-stimulated macrophages. The rhamnetin treatment group showed reductions in the lipid profile and levels of parameters of liver function compared to ApoE-/- mice. The levels of inflammatory cytokines and oxidative stress were reduced in the aortic tissue of the rhamnetin treatment group compared to ApoE-/- mice. Treatment with rhamnetin ameliorated the expression of TLR-4 mRNA and components of the TLR-4 pathway in the aortic tissue of ApoE-/- mice. In conclusion, the results of this study suggest that rhamnetin treatment inhibits the inflammatory and pro-atherosclerosis pathways in ApoE-/- mice. Topics: Animals; Apolipoproteins E; Atherosclerosis; Inflammation; Macrophages; Mice; Mice, Knockout; Quercetin | 2021 |
The Dietary Flavonoid Rhamnetin Inhibits Both Inflammation and Excitotoxicity During Ethanol Withdrawal in Rat Organotypic Hippocampal Slice Cultures.
Ethanol (EtOH) causes neurotoxicity via several mechanisms including neuroinflammation (during EtOH exposure), and excitotoxicity (during EtOH withdrawal [EWD]). Alpha7 nicotinic acetylcholine receptor (nAChR) selective agonists have the potential to reduce both. The aim of this study was to evaluate the anti-inflammatory and neuroprotective potential of rhamnetin, a dietary flavonoid with alpha7 nAChR selective activity, in an in vitro model of EtOH-induced neurotoxicity.. The anti-inflammatory and neuroprotective properties of rhamnetin were assessed in neonatal organotypic hippocampal slice cultures undergoing EWD (or not) and challenged with N-methyl-D-aspartate (NMDA) and/or lipopolysaccharide (LPS). Neurotoxicity was determined using propidium iodide uptake, and the inflammatory response was evaluated by measuring the release of tumor necrosis factor (TNF)-alpha (NO; quantified by ELISA) and nitric oxide (quantified by the Griess reaction) into culture media.. As predicted, rhamnetin reduced LPS-induced release of TNF-alpha and NO both under control conditions and during EWD. Additionally, rhamnetin had no effect on NMDA-induced neurotoxicity under control conditions, but significantly reduced NMDA toxicity during EWD. In contrast, rhamnetin had no effect on neurotoxicity induced by NMDA and LPS combined despite reducing TNF-alpha and NO levels under these conditions.. Rhamnetin is anti-inflammatory and neuroprotective during EWD and therefore has potential value in treating neurotoxicity caused by EtOH. Topics: Animals; Ethanol; Excitatory Amino Acid Agonists; Female; Flavonoids; Hippocampus; Inflammation; Inflammation Mediators; Male; Organ Culture Techniques; Quercetin; Rats; Rats, Sprague-Dawley; Substance Withdrawal Syndrome | 2015 |