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Abstract
Unlabelled:
This study was investigated on the mechanism of the sedative state, tranquilization induced by bradykinin (BK) and kallikrein (KAL). The drugs used in this study were as follows: KAL as endogenous BK promoter; prostaglandins (PGs) as a material of analogous action of BK; indomethacin and mepacrine as the inhibitors of PG-synthesis; eugenol as the OH- scavenger and the PGE-synthesis potentiator; angiotensin converting enzyme inhibitor as BK potentiator B. All drugs were dissolved in Hartmann's solution (lactate Ringer's solution) and 10 microliters of solution was injected into the lateral ventricle of rats, according to the Myers' procedure. Then, the rat behavior was estimated, by means of monitoring spontaneous movement. A high performance liquid chromatography (HPLC) was used for detecting alteration of monoamines and prostaglandins in the rat brain on sedative state after BK or KAL injection.
Results:
1) A 2-phase alteration of spontaneous movement was occurred within 30 min after BK or KAL icv-injection with behavioral specificity as follows: two exciting states and one sedative state. 2) A great increase of spontaneous movement evoked by BK or KAL was accompanied by exciting state as follows: jumping, wet dog response, struggle and scratching response, rearing and exploration. 3) A great decrease of spontaneous movement evoked by BK or KAL was accompanied with sedative state as follows: crouching with piloerection and closed eyes, catalepsy, preening and moisturizing and grooming. 4) PGE1 icv-injection was also carried out to clarify the involvement in the BK- or KAL-induced behavioral alteration. Consequently caused PGE1 the similar result to BK or KAL. 5) ACEI elongated and enhanced the exciting state or sedative state evoked by BK or KAL. 6) It was clear that BK reduced levels of monoamines in the rat hypothalamus: levels of norepinephrine(NE), epinephrine(E), dopamine(DA) and 5-hydroxytryptamine (5-HT) were decreased to 72.5%, 53.5%, 71.2% and 75.0% of control, respectively. Reduction of catecholamines in the hypothalamus was produced by increase of PGs and subsequently occurred sedative state of rats. 7) BK- or KAL-induced exciting state was enhanced by PG- synthesis inhibitor, especially the cyclo-oxygenase inhibitor indomethacin, but the sedative state was weakened. On the contrary, eugenol, an OH- scavenger, elongated and intensified the sedative state. Detection with HPLC showed remarkable increase of levels of PGs in the rat brain during the sedative state: the level of PGE2 was 27.5% increase of control and the level of PGE2 alpha was also 54.8% increase of control, respectively.
... In experimental diabetes, EUG improves vascular and neuronal complications and suppresses the transmission of action potential in sciatic nerves [39]. It also elongates the kallikrein-and bradykinin-induced tranquilization [135]. EUG is a good medicine for Alzheimer's disease (AD) and depression. ...
The biologically active phytochemicals are sourced from edible and medicinally important plants and are important molecules being used for the formulation of thousands of drugs. These phytochemicals have great benefits against many ailments particularly the inflammatory diseases or oxidative stress-mediated chronic diseases. Eugenol (EUG) is a versatile naturally occurring molecule as phenolic monoterpenoid and frequently found in essential oils in a wide range of plant species. EUG bears huge industrial applications particularly in pharmaceutics, dentistry, flavoring of foods, agriculture, and cosmeceutics. It is being focused recently due to its great potential in preventing several chronic conditions. The World Health Organization (WHO) has declared EUG as a nonmutant and generally recognized as safe (GRAS) molecule. The available literature about pharmacological activities of EUG shows remarkable anti-inflammatory, antioxidant, analgesic, and antimicrobial properties and has a significant effect on human health. The current manuscript summarizes the pharmacological characteristics of EUG and its potential health benefits.
... In sensory system, eugenol is acts as neuroprotective against excitotoxicity, ischemia and amyloid-β peptide, restrains the conduction of activity potential in sciatic nerves and enhances neuronal and vascular intricacies in exploratory diabetes [3][4][5][6][7] . Eugenol has been reported to stretch bradykinin and kallikrein incited sedation 8 . Old Chinese pharmacopeias uncovered that most natural cures demonstrated for Alzheimer illness (AD or indications reminiscent of AD) contains the organic Rhizoma acori graminei which is rich in eugenol 9 . ...
Metabotrophic glutamate receptors were expressed abnormal in the neurodegenerative diseases. The negative regulation of the abnormal expression induce glutamate excitotoxicity has connected to interminable neurodegenerative issues for example, amyotrophic parallel sclerosis, multiple sclerosis and Parkinson's disease. The molecular target metabrophic glutamate receptors were modulated and regulated by the potent medicinal compounds. Eugenol is a medicinal value rich compound found in the buds and leaves of clove (Syzygium aromaticum (L.) Merrill and Perry), which has been accounted to have antioxidant, anticancer and neuroprotective activity. In this present study the Eugenol compound was evaluated for the neuroprotective activity through molecular docking and molecular property prediction. The eugenol compound was optimized and prepared as ligand molecule using ligprep tool. Similarly the glutamate receptors were prepared for molecular docking through auto dock tool. Prelimarily, the eugenol was evaluated for the molecular properties and drug likeliness sore. The duglikeliness score -0.60 of eugenol indicated the highest score and confirmed as potent drug like compound. Totally ten glutamate receptors were chosen and docked with eugenol ligand molecule. Among the receptors 2e4y, 3ks9, 2wjw and 3lmk were significantly inhibited by eugenol. 2e4y and 3ks9 achieved the best docking frequency (-28.01and -32.90) with atomic contact energy.
... In sensory system, eugenol is acts as neuroprotective against excitotoxicity, ischemia and amyloid-β peptide, restrains the conduction of activity potential in sciatic nerves and enhances neuronal and vascular intricacies in exploratory diabetes [3][4][5][6][7] . Eugenol has been reported to stretch bradykinin and kallikrein incited sedation 8 . Old Chinese pharmacopeias uncovered that most natural cures demonstrated for Alzheimer illness (AD or indications reminiscent of AD) contains the organic Rhizoma acori graminei which is rich in eugenol 9 . ...
Metabotrophic glutamate receptors were expressed abnormal in the neurodegenerative diseases. The negative regulation of the abnormal expression induce glutamate excitotoxicity has connected to interminable neurodegenerative issues for example, amyotrophic parallel sclerosis, multiple sclerosis and Parkinson's disease. The molecular target metabrophic glutamate receptors were modulated and regulated by the potent medicinal compounds. Eugenol is a medicinal value rich compound found in the buds
and leaves of clove (Syzygium aromaticum (L.) Merrill and Perry), which has been accounted to have antioxidant, anticancer and neuroprotective activity. In this present study the Eugenol compound was evaluated for the neuroprotective activity through molecular docking and molecular property prediction. The eugenol compound was optimized and prepared as ligand molecule using ligprep tool. Similarly the glutamate receptors were prepared for molecular docking through auto dock tool. Prelimarily, the eugenol
was evaluated for the molecular properties and drug likeliness sore. The duglikeliness score -0.60 of eugenol indicated the highest score and confirmed as potent drug like compound. Totally ten glutamate receptors were chosen and docked with eugenol ligand molecule. Among the receptors 2e4y, 3ks9, 2wjw and 3lmk were significantly inhibited by eugenol. 2e4y and 3ks9 achieved the best docking frequency (-28.01and -32.90) with atomic contact energy.
... Eugenol interfered with rat phrenic nerve transmission due to membranestabilizing (local anesthetic) effect at low concentrations (Brodin and Roed 1984). Experimental data on rodents suggest that eugenol has anxiolytic (Yazaki 1989), anti-epileptic (Mü ller et al. 2006, and antidepression-like (Irie et al. 2004) activities. Anti-stress effects of eugenol, by reducing stress-induced increases in protein cauterization and fluidity of synaptosomal membranes, have been reported (Sen et al. 1992). ...
Stress is the leading psychopathological cause for several mental disorders. Physiological and psychological responses to stress are mediated by the hypothalamic?pituitary?adrenal (HPA), sympathoadrenal system (SAS), and brain monoaminergic systems (BMS). Eugenol is reported to substantially modulate brain functions by regulating voltage-gated cation channels and release of neurotransmitters. This study was designed to evaluate the anti-stress effect of eugenol in the 4-h restraint model using rats. Ulcer index was measured as a parameter of the stress response. HPA axis and the SAS were monitored by estimating plasma corticosterone and norepinephrine (NE), respectively. Analysis of NE, serotonin (5-HT), dopamine, and their metabolites in discrete brain regions was performed to understand the role of BMS in the anti-stress effect of eugenol. Stress exposure increased the ulcer index as well as plasma corticosterone and NE levels. Eugenol pretreatment for 7 days decreased the stress-induced increase in ulcer index and plasma corticosterone but not NE levels, indicating a preferential effect on the HPA axis. Furthermore, eugenol showed a ?U?-shaped dose?response curve in decreasing ulcer index and plasma corticosterone levels. Eugenol also reversed the stress-induced changes in 5-HT levels in all brain regions, whereas NE levels were reversed in all brain regions except hippocampus. These results suggest that eugenol possesses significant anti-stress activity in the 4-h restraint model and the effect is due to modulation of HPA and BMS.
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