Methyl jasmonate attenuates memory dysfunction and decreases brain levels of biomarkers of neuroinflammation induced by lipopolysaccharide in mice

Umukoro, Solomon; Eduviere, Anthony T.

doi:10.1016/j.brainresbull.2017.04.002

Cited by 24 publications

(25 citation statements)

References 36 publications

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“…In this study, MeJA was effective as anti-inflammatory, notably at the dose of 300 mg·kg −1 . The anti-inflammatory activity of MeJA was already shown previously in LPS-activated murine macrophages (RAW264.7) [ 8 – 10 ] and in vivo in the brain of mice with LPS-induced neuroinflammation [ 21 ]. Our results reveal that MeJA is additionally effective on articular and systemic inflammation, especially in the liver of rats with adjuvant-induced arthritis.…”

Section: Discussionmentioning

confidence: 79%

“…The anti-inflammatory mechanism of MeJA has not yet been completely clarified, but it is known that it suppresses NF- κ B-mediated expression of proinflammatory enzymes and cytokines. MeJA inhibited the production of prostaglandin E, TNF- α , IL-1, and IL-6 as well as the expression of iNOS, COX-2, and NF- κ B in the brain of mice with LPS-induced neuroinflammation and LPS-stimulated RAW267.4 cells [ 8 , 21 ]. In addition, MeJA was reported to attenuate activation of NF- κ B by suppressing degradation of its inhibitor I kappa B-alpha (I κ B- α ) [ 21 ].…”

Section: Discussionmentioning

confidence: 99%

“…MeJA inhibited the production of prostaglandin E, TNF- α , IL-1, and IL-6 as well as the expression of iNOS, COX-2, and NF- κ B in the brain of mice with LPS-induced neuroinflammation and LPS-stimulated RAW267.4 cells [ 8 , 21 ]. In addition, MeJA was reported to attenuate activation of NF- κ B by suppressing degradation of its inhibitor I kappa B-alpha (I κ B- α ) [ 21 ]. Evidence from studies with methyl dehydrojasmonate, a structural analog of MeJA, suggests that MeJA may in addition downregulate miR-155, which is elevated in synovial fibroblasts from rheumatoid arthritis patients and LPS-stimulated RAW267.4 cells [ 9 , 42 ].…”

Section: Discussionmentioning

confidence: 99%

“…Anti-inflammatory actions of MeJA were mainly demonstrated in isolated cells, but in vivo approaches have seldom been reported. A recent study showed that increased brain levels of prostaglandin E, TNF- α , and IL-1 in LPS-induced neuroinflammation in mice were reduced by intraperitoneally administered MeJA, which also suppressed COX-2, iNOS and NF- κ B expression [ 21 ]. However, these actions refer specifically to neuroinflammation and so far no other systemic manifestation has been evaluated.…”

Section: Introductionmentioning

confidence: 99%

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Anti‐Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats

Sá‐Nakanishi

Soni-Neto

Moreira

et al. 2018

Oxidative Medicine and Cellular Longevity

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Methyl jasmonate (MeJA) is a fatty acid-derived cyclopentanone which shares structural similarities with prostaglandins and has been under study as a promising anti-inflammatory agent. This study investigated the actions of MeJA on systemic inflammation and oxidative status in rats with adjuvant-induced arthritis, a model for rheumatoid arthritis. MeJA (75 to 300 mg·kg−1) was administrated orally during 18 days after arthritis induction with Freund's adjuvant. Articular and systemic inflammation was greatly increased in arthritic rats, likewise the oxidative stress in plasma and liver. The hepatic glucokinase activity and glycolysis were increased in arthritic rats. MeJA decreased most inflammatory parameters and abolished the increased protein carbonylation in plasma and liver, diminished the increased hepatic ROS content, and restored the hepatic GSH/GSSG ratio in arthritic rats. However, the MeJA treatment decreased the hepatic glucokinase activity and glycolysis and stimulated mitochondrial ROS production in healthy and arthritic rats. Oxygen uptake was increased by MeJA only in livers from treated arthritic rats. This action may bear relation to the increased activity of mitochondrial NADP+-dependent enzymes to provide reducing equivalents for the glutathione cycle. These beneficial effects, however, are associated with a decreased glucose flux through the glycolysis in the liver of arthritic and healthy rats.

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Section: Discussionmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Anti‐Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats

Sá‐Nakanishi

Soni-Neto

Moreira

et al. 2018

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“… 19 Recent studies have shown that the expression of Aβ, progressive neurodegeneration, loss of learning and memory, and the release of neuroinflammatory mediators have been detected in LPS-induced animals. 20 , 21 …”

Section: Introductionmentioning

confidence: 99%

Hemp (Cannabis sativa L.) Seed Phenylpropionamides Composition and Effects on Memory Dysfunction and Biomarkers of Neuroinflammation Induced by Lipopolysaccharide in Mice

Zhou

Wang

et al. 2018

ACS Omega

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Hempseed has achieved a growing popularity in human nutrition, particularly regarding essential amino acids and fatty acids. The multiple positive attributes of hempseed have led to the further study of its constituents. In this study, hempseed extract containing phenylpropionamides (TPA) was obtained and its chemical profile and content were obtained using high-performance liquid chromatography technology based on previous study. The anti-neuroinflammatory effect of TPA extract was evaluated using a lipopolysaccharide (LPS)-induced mouse model. Fourteen phenylpropionamides (TPA) were identified in the obtained extract with a total content of 233.52 ± 2.50 μg/mg extract. In mice, TPA prevented the learning and spatial memory damage induced by LPS. Increased brain levels of IL-1β, IL-6, and TNF-α in the LPS-induced mice were reduced by TPA treatment. Furthermore, TPA attenuated LPS-induced hippocampal neuronal damage in mice. This study demonstrates the nutraceutical potential of hempseed from a neuroprotective perspective.

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Probable mechanisms involved in the antipsychotic-like activity of methyl jasmonate in mice

Annafi

Aluko

Eduviere

et al. 2017

Naunyn-Schmiedeberg's Arch Pharmacol

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Psychosis is a chronic neuropsychiatric disorder that affects millions of individuals worldwide and impairs the quality of life and productivity of the patients. The clinical efficacy of antipsychotic drugs has been compromised by adverse effects, relapse, and therapeutic failures, thus necessitating search for alternative agents. Methyl jasmonate (MJ) is a bioactive compound reported to have beneficial effects in various neurological disorders. This study was undertaken to investigate the antipsychotic-like effects of MJ in mice. Male Swiss mice were pretreated intraperitoneally with MJ (25-100 mg/kg) or vehicle (10 mL/kg) 60 min prior to bromocriptine (5 mg/kg) or acute injection of ketamine (10 mg/kg). Thereafter, each mouse was observed for stereotype behaviors for 2 min at 10, 15, 20, 30, and 45 min post-bromocriptine injection. Another set of mice received MJ (25-100 mg/kg) or vehicle (10 mL/kg) 60 min after chronic ketamine injection (20 mg/kg, i.p) once daily for 14 consecutive days. Afterwards, locomotor activity and memory function in this sequence were evaluated using open field and Y-maze tests. The levels of malondialdehyde (MDA) and glutathione (GSH) and activity of catalase and superoxide dismutase (SOD) in the brain were determined. MJ significantly inhibited stereotypy behavior induced by bromocriptine or acute ketamine injection, which suggest antipsychotic-like activity. It also attenuated hyper-locomotion and memory deficits induced by chronic injection of ketamine in mice. The increased oxidative stress as shown by the altered brain levels of MDA, GSH, and activity of antioxidant enzymes induced by chronic injection of ketamine was reduced by MJ. Taken together, these findings suggest that MJ demonstrated antipsychotic-like property via mechanism related to its antioxidant property and interference with dopaminergic neurotransmission.

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Methyl jasmonate attenuates memory dysfunction and decreases brain levels of biomarkers of neuroinflammation induced by lipopolysaccharide in mice

Cited by 24 publications

References 36 publications

Anti‐Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats

Anti‐Inflammatory and Antioxidant Actions of Methyl Jasmonate Are Associated with Metabolic Modifications in the Liver of Arthritic Rats

Hemp (Cannabis sativa L.) Seed Phenylpropionamides Composition and Effects on Memory Dysfunction and Biomarkers of Neuroinflammation Induced by Lipopolysaccharide in Mice

Probable mechanisms involved in the antipsychotic-like activity of methyl jasmonate in mice

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