Evaluation of adaptogenic-like property of methyl jasmonate in mice exposed to unpredictable chronic mild stress

Umukoro, Solomon; Aluko, Oritoke Modupe; Eduviere, Anthony T.; Owoeye, Olatunde

doi:10.1016/j.brainresbull.2015.11.016

Cited by 35 publications

(32 citation statements)

References 41 publications

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“…Oxidative stress contributes to the pathophysiologic cascade relating with hippocampus injury [ 30 ]. Similarly, cumulative evidence indicates that oxidative stress in the hippocampus exerts a vital role in CUMS-induced pathogenesis of rodents [ 31 – 37 ]. Lowered antioxidant enzyme activity within the central nervous system may impair protection against reactive oxygen species (ROS), leading to damage to intracellular structure such as DNA, fatty acid, and protein [ 38 – 41 ].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress‐Induced Oxidative Stress in Hippocampus by Upregulation of BDNF‐TrkB Pathway

Zou

Wang

et al. 2016

Oxidative Medicine and Cellular Longevity

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Chronic unpredictable mild stress (CUMS) induces hippocampal oxidative stress. H2S functions as a neuroprotectant against oxidative stress in brain. We have previously shown the upregulatory effect of H2S on BDNF protein expression in the hippocampus of rats. Therefore, we hypothesized that H2S prevents CUMS-generated oxidative stress by upregulation of BDNF-TrkB pathway. We showed that NaHS (0.03 or 0.1 mmol/kg/day) ameliorates the level of hippocampal oxidative stress, including reduced levels of malondialdehyde (MDA) and 4-hydroxy-2-trans-nonenal (4-HNE), as well as increased level of glutathione (GSH) and activity of superoxide dismutase (SOD) in the hippocampus of CUMS-treated rats. We also found that H2S upregulated the level of BDNF and p-TrkB protein in the hippocampus of CUMS rats. Furthermore, inhibition of BDNF signaling by K252a, an inhibitor of the BDNF receptor TrkB, blocked the antioxidant effects of H2S on CUMS-induced hippocampal oxidative stress. These results reveal the inhibitory role of H2S in CUMS-induced hippocampal oxidative stress, which is through upregulation of BDNF/TrkB pathway.

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Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress‐Induced Oxidative Stress in Hippocampus by Upregulation of BDNF‐TrkB Pathway

Zou

Wang

et al. 2016

Oxidative Medicine and Cellular Longevity

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“…Although MJ is widely used to treat depression, nervousness, and improve memory in aromatherapy, the finding that MJ demonstrated sedative effect and enhanced GABA currents [Hossain et al, ] provided the first experimental evidences supporting a mechanistic basis for its therapeutic benefits in neuropsychiatric disorders. Moreover, MJ demonstrated adaptogenic, antiamnesic, and antipsychotic activities in rodents [Eduviere et al, ; Umukoro et al, ; Annafi et al, ] and exhibited antidepressant‐like activity in mice subjected to acute stress models of forced swimming (FST) and tail suspension (TST) tests. It also attenuated depressive‐like symptoms induced by lipopolysaccharide in mice [Umukoro et al, ; Adebesin et al, ].…”

Section: Introductionmentioning

confidence: 99%

Methyl Jasmonate Ameliorates Unpredictable Chronic Mild Stress‐Induced Behavioral and Biochemical Alterations in Mouse Brain

Adebesin

Ajayi

Olonode

et al. 2017

Drug Development Research

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Preclinical Research The effects of methyl jasmonate (MJ; 5, 10, 20 mg/kg, i.p), a natural product widely used for the relief of stress, depression, and exhaustion on unpredictable chronic mild stress (UCMS)-induced depression-like behaviors in mice was assessed and compared to those of imipramine (IMP; 10 mg/kg, i.p). MJ and IMP were given 30 min before exposure to UCMS with the procedure repeated daily for 2 weeks; 24 h after the stress session, the tail suspension test (TST) and sucrose preference test were assessed. MJ decreased immobility time in the TST and reversed impaired intake of sucrose relative to the stressed control suggesting antidepressant-like activity. MJ also reduced UCMS-induced increases in corticosterone and MDA (malondialdehyde) levels and attenuated UCMS-induced decreases in GSH and TNF-α levels and SOD activity. These findings suggest that MJ attenuated UCMS-induced depressive-like behaviors through decreased levels of corticosterone and decreasing oxidative stress and neuroinflammation in mouse brain.Drug Dev Res 78 : 381-389, 2017. © 2017 Wiley Periodicals, Inc.

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“…The formed alkyl radicals cause rearrangement and forms conjugated dienes and start cascades of autocatalytic lipid peroxidation. 58 The inflammatory cascades produce reactive oxygen species and their derivatives are involved in several degenerative reactions in a biological system. Several finding showed that MeJA has significantly reduced the oxidative burden, a free radical abundance which is responsible for inflammatory cascades by the restoration of endogenous anti-oxidant enzymes, i.e., catalase, glutathione, superoxide dismutase, etc., the depletion of endogenous antioxidant enzymes creates imbalance and causes ROS mediated cellular damage.…”

Section: Inhibition Of Oxidative Stressmentioning

confidence: 99%

Molecular mechanism of plant stress hormone methyl jasmonate for its anti-inflammatory activity

Gunjegaonkar

Shanmugarajan

2019

Plant Signaling & Behavior

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Plant stress hormones (Phytohormones/PTH) are abundantly present in numerous vascular plants. Several classes of plant stress hormones like auxins (AU) & gibberellins (GA), cytokinins (CK), abscisic acid (ABA), ethylene (ET), salicylic acid (SA), jasmonates (JA), brassinosteroids (BR) and strigolactones are synthesized within specialized plant cells. Among them, jasmonate are prominent class of stress hormones involved in survival of plants in stressful conditions. Methyl jasmonate (MeJA) is ester of jasmonic acid is extensively studied for its potential clinical benefits. MeJA is used as an effective antimicrobial agent, food preservative, antioxidant in food and agricultural sectors. The clinical benefits of MeJA have been related to their prominent interactions with inflammatory NF-κB pathways, inhibition of enzymes, gene expression for synthesis of inflammatory mediators, signaling molecules, oxidative stress and modulation of pain perception/nociceptive responses. The objective of the present review is to provide an cohesive relation of MeJA in inflammation with reference to past and recent in-vivo and in-vitro investigations in broad perspectives.

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Evaluation of adaptogenic-like property of methyl jasmonate in mice exposed to unpredictable chronic mild stress

Cited by 35 publications

References 41 publications

Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress‐Induced Oxidative Stress in Hippocampus by Upregulation of BDNF‐TrkB Pathway

Hydrogen Sulfide Protects against Chronic Unpredictable Mild Stress‐Induced Oxidative Stress in Hippocampus by Upregulation of BDNF‐TrkB Pathway

Methyl Jasmonate Ameliorates Unpredictable Chronic Mild Stress‐Induced Behavioral and Biochemical Alterations in Mouse Brain

Molecular mechanism of plant stress hormone methyl jasmonate for its anti-inflammatory activity

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