Background: The aim of this study was to compare the expression of interleukin-1β (IL-1β), neuronal nitric oxide synthase (nNOS) and inducible nitric oxide synthase (iNOS) in the prefrontal cortex (PFC), hippocampus (HIP) and hypothalamus (HT) during chronic crowding (CS) (psychosocial) and restraint (RS) (physico-psychological) stress. Adaptational changes of these stress mediators to a subsequent acute RS, in two models of chronic stress were investigated.
Methods: Rats were crowded (24 in one cage) or restrained in metal tubes for 10min twice a day for 3, 7, and 14 consecutive days and decapitated. For determination of adaptational changes the chronically crowded and restrained rats 24h after the last stress session were subjected to a single 10min RS. The IL-1β, nNOS and iNOS protein levels in brain structures samples were analyzed by Western blot procedure.
Results: Chronic CS for 3days did not markedly change the subsequent acute stress induced expression of nNOS, iNOS and IL-1β protein level in PFC and iNOS protein level in HT. CS markedly decreased the expression of nNOS, iNOS and IL-1β in HIP. By contrast, parallel chronic RS, significantly increased the subsequent acute stress-induced expression of iNOS and IL-1β in PFC and considerably increased iNOS level in HT.
Conclusion: Chronic psychosocial stress, may protect against possible harmful action of hyperproduction of iNOS and iNOS derived nitric oxide (NO) mainly in PFC and HIP. By contrast, chronic physico-psychosocial stress may strongly potentiate additional stress-induced harmful effects of NOS and IL-1β hyperproduction.
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http://dx.doi.org/10.1016/j.pharep.2016.09.003 | DOI Listing |
Clin Sci (Lond)
January 2025
Center for Interdisciplinary Research in Biology, College de France, Institut National de la Santé et de la Recherche Médicale, Paris, France.
Apelin, a (neuro) vasoactive peptide, plays a prominent role in controlling water balance and cardiovascular functions. Apelin and its receptor co-localize with vasopressin in magnocellular vasopressinergic neurons. Apelin receptors (Apelin-Rs) are also expressed in the collecting ducts of the kidney, where vasopressin type 2 receptors are also present.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pulmonary and Critical Care Medicine, Shanghai Fifth People's Hospital, Fudan University, Shanghai, 200240, China.
Asthma, a widespread chronic inflammatory disease can contribute to different degrees of lung function damage. The objective of this study is to explore the potential effects of nitric oxide synthase (NOS) inhibitors in asthma using mice model induced by ovalbumin (OVA). BALB/c mice were treated with OVA to establish an asthma model.
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Department of Zoology, Faculty of Science, Alexandria University, Alexandria, 21515, Egypt.
Exaggerated neuronal excitation by glutamate is a well-known cause of excitotoxicity, a key factor in numerous neurodegenerative disorders. This study examined the neurotoxic effect of monosodium glutamate (MSG) in the brain cortex of rats and focused on assessing the potential neuroprotective effects of omega-3 polyunsaturated fatty acids (ω-3 PUFAs). Four groups of adult male rats (n = 10) were assigned as follows; normal control, ω-3 PUFAs (400 mg/kg) alone, MSG (4 mg/g) alone, and MSG plus ω-3 PUFAs (4 mg/g MSG plus 400 mg/kg ω-3 PUFAs).
View Article and Find Full Text PDFCurr Drug Metab
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Pharmacological Research Center of Medicinal Plants, Mashhad University of Medical Sciences, Mashhad, Iran.
Quercetin (QE), a particular flavonoid, is well known for its medicinal effects, including anti-oxidant, hypoglycemic, and anti-inflammatory effects. In this review, the findings of QE effects on diabetes STZinduced, alloxan-induced, and its complications have been summarized with a particular focus on in vitro, in vivo, and clinical trials. Consequently, QE mediates several mechanisms, including ameliorating tumor necrosis factor (TNF)-α, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), interleukin (IL)-1β, IL-8, and IL-10 expression, increasing insulin glucose uptake to inhibit insulin resistance.
View Article and Find Full Text PDFFront Physiol
January 2025
College of Dental Medicine, Lincoln Memorial University, Harrogate, TN, United States.
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