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Central Nervous System Effects of Essential Oil Compounds
Published in K. Hüsnü Can Başer, Gerhard Buchbauer, Handbook of Essential Oils, 2020
Elaine Elisabetsky, Domingos S. Nunes
Oleamide 34 is part of a brain lipid family that induces sleep (Cravatt et al., 1995). Systemic and icv administration of 34 to rats and mice markedly decreased sleep latency without changing other sleep parameters (Basile et al., 1999; Mendelson, 2001). When the major metabolizing enzyme for 34 (fatty acyl amide hydrolase, type I) is administered intraventricularly, sleep latency is reduced and total sleep is increased (Mendelson, 2001). In one study, acute and the subchronic (15 days) centrally administered oleamide increased REMS in rats, without affecting waking and NREM sleep. No abstinence effects on the sleep–waking cycle were observe after drug cessation (Herrera-Solís et al., 2010). Another study found that 50 administered systemically increased slow-wave sleep and decreased wakefulness and sleep latency, with no effects on REM sleep. The oleamide-induced increase in slow-wave sleep was prevented by 5-HT reuptake inhibitors (Yang et al., 2003). Research has found that 34 acts as a full cannabinoid receptor agonist (Leggett et al., 2004), and at least part of its hypnotic action involves the CB1 receptor system (Mendelson and Basile, 1999). A very well thought of and elegant series of experiments generated data to show that the cis isomer of oleamide is a stereoselective modulator of voltage-gated Na+ channel and GABAA receptor complex (Verdon et al., 2000). The mechanism is consistent with the hypno-sedative effects observed in vivo for cis-oleamide and its anticonvulsant effects (Verdon et al., 2000). Therefore, 34 effects on CB1 are compounded with other properties, such as the allosteric modulation of other receptors and fatty acid amide hydrolase inhibition.
The Role of Endogenous Sleep-promoting Substances
Published in Clete A. Kushida, Sleep Deprivation, 2004
Ferenc Obal, Fabio Garcia-Garcia, James M. Krueger
A few additional substances are implicated in sleep regulation, although the evidence for their sleep role is substantially less than that of the molecules discussed above. Oleamide is an unsaturated fatty acid that was isolated from the CSF of a sleep-deprived cat (152). Oleamide is structurally related to the endogenous cannabinoid anandamide, and it is possible that oleamide promotes NREM sleep via cannabinoid receptors directly or indirectly by inhibiting anan-damide metabolism (153). Cortistatin is a peptide displaying strong homology with somatostatin. It is an inhibitory neurotransmitter in the cerebral cortex and in the hippocampus (154). Cortistatin seems to promote NREM sleep, but the sleep responses have not been thoroughly studied. Cholecystokinin (CCK) is a peptide hormone released from the duodenum in response to fats and proteins, and might be involved in the mediation of postprandial sleep. CCK promotes NREM sleep (155). The action is peripheral and might be mediated by vagal sensory neurons. Insulin is a peptide hormone released from the pancreas that stimulates glucose uptake by skeletal muscle and adipocytes and has a fundamental role in the regulation of metabolism of sugar, lipid, and protein, and in tissue growth. Promotion of NREM sleep was reported after intracerebroventricular administration of insulin in rats (156). However, the evidence is scarce implicating insulin in sleep regulation, and the sleep-promoting activity of intracerebral insulin might be mediated by IGF-1 receptors (157). Nitric oxide (NO) is also implicated in sleep regulation (158). The findings linking NO to regulation of NREM sleep are controversial (159), whereas the results are consistent that suggest that NO stimulates REM sleep by acting in the pedunculopontine tegmen-tum in the brainstem (160). Interestingly, neural NO synthase knockout mice have less REM sleep whereas inducible NO synthase knockout mice have more REM sleep (161).
Metabolomics approach of Symphyotrichum squamatum ethanol extract and its nano-Ag formulation protective effect on gastric ulcer via bio-chemical and pathological analyses
Published in Biomarkers, 2023
Heba A. Hassan, Iriny M. Ayoub, Tamer I. M. Ragab, Sherif M. Afifi, Abd El-Nasser G. El-Gendy, Abdel Razik H. Farrag, Ahmed M. Abd-ELGawad, Mohamed Farag, Abdelsamed Elshamy, Naglaa M. Ammar
In this study, potential biomarkers associated with various metabolic pathways related to GU were identified using metabolomics in disease rat serum. According to multivariate data analysis, lipids, energy metabolism, pyrimidine and phosphatidylinositol signalling system pathway were the most influential. Interestingly, fatty acid amides (FAAs) form a group of endogenous lipid mediators of growing interest in their biological role. FAAs can be divided into two classes: fatty acid primary amides and N-acyl-ethanolamines (Hiley and Hoi 2007). An interesting result of the present study is that oleamide, which is a primary fatty acid amide was lowered in the serum of ulcer model group (Figure 4B). Oleamide is the prototype long-chain primary fatty acid amide lipid messenger (Mueller and Driscoll 2009) produced from oleoylglycine, or from the direct amidation of oleic acid via oleoyl coenzyme A by cytochrome c using ammonia as the nitrogen source. In a prior study, it was reported that ulcer model group showed reduced oleamide levels related to invasive inflammation (Ammar et al.2022).
Gastro-protective effect of Artemisia Sieberi essential oil against ethanol-induced ulcer in rats as revealed via biochemical, histopathological and metabolomics analysis
Published in Biomarkers, 2022
Naglaa M. Ammar, Heba A. Hassan, Rania F. Ahmed, Abd El-Nasser G. El-Gendy, Ahmed M. Abd-ElGawad, Abdel Razik H. Farrag, Mohamed A. Farag, Abdelsamed I. Elshamy, Sherif M. Afifi
Aside from these established biomarkers known in gastric ulcers, metabolomics analysis of rat serum revealed potential novel biomarkers involved in some metabolic pathways related to GU (Figure 5). Among these, fatty acids and fatty acyl amides were most influential as revealed from multivariate data analysis (Figures 2 and 5) exemplified by a decrease in oleamide, a fatty acid amide in the serum of ulcer model group (Figure 3). Oleamide is the prototype long-chain primary fatty acid amide lipid messenger (Mueller and Driscoll 2009) produced from oleoylglycine, or from the direct amidation of oleic acid via oleoyl coenzyme A by cytochrome c (Mueller and Driscoll 2009).