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      • KCI등재

        Methyl Jasmonate: Behavioral and Molecular Implications in Neurological Disorders

        Oritoke Modupe Aluko,Joy Dubem Iroegbu,Omamuyovwi Meashack Ijomone,Solomon Umukoro 대한정신약물학회 2021 CLINICAL PSYCHOPHARMACOLOGY AND NEUROSCIENCE Vol.19 No.2

        Methyl jasmonate (MJ) is a derivative of the jasmonate family which is found in most tropical regions of the world and present in many fruits and vegetables such as grapevines, tomato, rice, and sugarcane. MJ is a cyclopentanone phytohormone that plays a vital role in defense against stress and pathogens in plants. This has led to its isolation from plants for studies in animals. Many of these studies have been carried out to evaluate its therapeutic effects on behavioral and neurochemical functions. It has however been proposed to have beneficial potential over a wide range of neurological disorders. Hence, this review aims to provide an overview of the neuroprotective properties of MJ and its probable mechanisms of ameliorating neurological disorders. The information used for this review was sourced from research articles and scientific databases using ‘methyl jasmonate’, ‘behavior’, ‘neuroprotection’, ‘neurodegenerative dis-eases’, and ‘mechanisms’ as search words. The review highlights its influences on behavioral patterns of anxiety, ag-gression, depression, memory, psychotic, and stress. The molecular mechanisms such as modulation of the antioxidant defense, inflammatory biomarkers, neurotransmitter regulation, and neuronal regeneration, underlying its actions in man-aging neurodegenerative diseases like Alzheimer’s and Parkinson’s diseases are also discussed. This review, therefore, provides a detailed evaluation of methyl jasmonate as a potential neuroprotective compound with the ability to modify behavioral and molecular biomarkers underlying neurological disorders. Hence, MJ could be modeled as a guided treat-ment for the management of brain diseases.

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        Monosodium glutamate induces memory and hepatic dysfunctions in mice: ameliorative role of Jobelyn® through the augmentation of cellular antioxidant defense machineries

        Omogbiya Adrian Itivere,Ben-Azu Benneth,Eduviere Anthony Taghogho,Eneni Aya-Ebi Okubo,Nwokoye Prisilla O.,Ajayi Abayomi Mayowa,Umukoro Solomon 한국독성학회 2021 Toxicological Research Vol.37 No.3

        This study investigated the effect of high doses of monosodium glutamate (MSG), a known food additive on hepatic, memory and locomotor functions in mice, and the ameliorative potentials of Jobelyn ® (JB), a unique dietary supplement. Twenty four male Swiss mice divided into 4 groups (n = 6) were given MSG (2, 4 and 8 g/kg) or normal saline (10 mL/kg) orally for 14 days. In the intervention study, another set of 30 male Swiss mice distributed into 5 groups (n = 6) received normal saline, MSG (8 g/kg) alone or in combination with JB (5, 10 and 20 mg/kg) orally, for 14 days. Memory and locomotor functions as well as brain oxido-nitrergic stress biomarkers were then assessed in both studies. The hepatic oxido-nitrergic stress biomarkers, liver enzymes functions and histomorphology of the liver were also assessed. MSG (2, 4 and 8 g/kg) produced memory dysfunction, hyperlocomotion, increased malondialdehyde and nitrite levels accompanied by decreased antioxidant status in the brain and hepatic tissues. MSG-treated mice had increased hepatic enzyme activities (alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase) and distorted cyto-architectural integrity of the liver. These findings further suggest that MSG compromised hepatic functioning, which might also contribute to its neurotoxicity. However, JB (5, 10 and 20 mg/kg, p.o) attenuated the memory deficit, hyperlocomotion, increased oxido-nitrergic stress responses in the brain and hepatic tissues induced by MSG (8 g/kg, p.o). JB also normalized hepatic enzymes activities and histomorphological changes in MSG-treated mice. Taken together, JB mitigated MSG-induced toxicity through mechanisms relating to enhancement of cellular antioxidant-machineries and normalization of hepatic enzymatic functions.

      • KCI등재

        Induction of apoptosis in activated RAW 264.7 cells and inhibition of pro-inflammatory mediators in rat air pouch by ethylacetate fraction of Ocimum gratissimum leaves

        Ajayi Abayomi Mayowa,Ben-Azu Benneth,Sikiru O. Balogun,Ruberlei Godinho de Oliveira,Umukoro Solomon,Domingos Tabajara de Oliveira,Olusegun G. Ademowo 경희대학교 융합한의과학연구소 2022 Oriental Pharmacy and Experimental Medicine Vol.22 No.3

        Ocimum gratissimum L. has attracted substantial consideration from researchers because of its anti-inflammatory uses in ethnomedicine in Sub-Saharan Africa and Asia. This study investigated the effect of flavonoid-rich ethylacetate fraction of O. gratissimum (EAFOg) in apoptosis induction of activated macrophages and inflammatory response in LPS-induced air pouch in rats. Apoptotic effect of EAFOg in LPS-stimulated RAW 264.7 cells was evaluated using flow cytometry after staining with annexin-V and 7-aminoactinomycin D. Its effects on inflammatory cells and mediators were investigated utilizing 6 day old subcutaneous air pouch-rats. Sterile saline (0.9%) or LPS (100 ng/mL) was injected into the air pouch on 6th day after EAFOg (25, 50 and 100 mg/kg) pretreatment. Rectal body temperature was recorded hourly for 5 h after LPS injection. Thereafter, the neutrophil count, nitrite, TNF-α, PGE2, nitrite, malondialdehyde and reduced glutathione (GSH) levels were determined in the pouch lavage. The activities of myeloperoxidase and superoxide dismutase (SOD) as well as immunohistochemical staining for cyclooxygenase-2 were also performed. EAFOg (10, 30 and 100 μg/mL) induced apoptosis in LPS-stimulated RAW 264.7 macrophages. The EAFOg reduced hyperthermia and decreased neutrophil counts, TNF-α, PGE2, nitrite, myeloperoxidase as well as cyclooxygenase-2 expression evoked by LPS in rats. It also reduced malondialdehyde, and increased GSH and SOD levels in LPS-induced air pouch in vivo. The results of this study suggest that the EAFOg

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