OKEOWO ORITOKE MODUPE
Publication
Methyl jasmonate is a naturally-occurring anti-stress plant hormone and has been shown to ameliorate the effects of acute and chronic stress in mice. The present study aimed to study the behavioral and biochemical mechanisms underlying the adaptogenic-like properties of methyl jasmonate.
Male Wistar albino rats were subjected to stressors of the unpredictable chronic mild stress (UCMS) paradigm for 28 days and treated with methyl jasmonate at 10, 25 and 50 mg/kg. Â Body and organ weights, behavioral and hematological parameters, as well as levels of biomarkers of oxidative stress were determined.
UCMS resulted in a progressive weight loss, hypertrophy of liver and adrenal gland, and atrophy of spleen and testes. An aberrant behavioral pattern as evident by swim endurance and post summing motor function tests were also observed in UCMS-subjected rats. Likewise, UCMS induced a deviant in hematological parameters. UCMS also significantly increased the levels of serum glucose, corticosterone, monoamine oxidase, lactate dehydrogenase, cholesterol, triglyceride, creatine kinase and blood urea nitrogen. There was also an alteration of oxidative stress markers viz malondialdehyde, superoxide dismutase, catalase, reduced glutathione, and nitric oxide arginase, ATPase, adenosine deaminase induced by UCMS.
Methyl jasmonate (10, 25 and 50 mg/kg) significantly ameliorated the UCMS-induced alterations in the body and organ weights. There was a significant amelioration of the UCMS-induced behavioral alterations by methyl jasmonate. Methyl jasmonate reversed the UCMS-induced suppression of erythrocytes, leukocytes, hemoglobin content, packed cell volume and lymphocyte count. Moreso, methyl jasmonate significantly reversed the alteration of oxidative stress markers induced by UCMS. Also, pretreatment with methyl jasmonate significantly attenuated UCMS-associated biochemical alterations, pathological outcomes, and oxidative stress.
The present findings showed the adaptogenic potential of methyl jasmonate in relation to the antioxidant systems implicating their therapeutic importance in stress-related disorders. Further investigations on the neurochemical and morphological mechanisms are being studied.
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 the search for alternative agents. Methyl jasmonate (MJ) is a bioactive compound reported to have beneficial effects on 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 behaviours 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 behaviour 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.
This study was undertaken to evaluate the adaptogenic-like activity of methyl jasmonate (MJ) in mice exposed to unpredictable chronic mild stress (UCMS).
Male Swiss mice were treated with MJ(25–100 mg/kg, i.p.) 30 min before exposure to UCMS daily for 14 days prior to testing for memory and anxiety. Thereafter, the blood glucose and serum corticosterone levels were estimated using glucometer and ELISA. The brain concentrations of malondialdehyde (MDA) and glutathione (GSH) were estimated using the spectrophotometer. Brain histology and the population of healthy neurons in the hippocampal regions were also assessed.
MJ reversed anxiety and memory impairment produced by UCMS, which suggest adaptogenic-like property. The reduction in the weight of adrenal gland and liver in MJ-treated groups further indicates adaptogenic activity. It further decreases the blood glucose and serum corticosterone levels in UCMS-mice. Also, MJ decreases the concentrations of MDA and elevated the levels of GSH in the brain of mice exposed to UCMS. Brain histology revealed that MJ attenuated UCMS-induced degeneration and death of neuronal cells in the pyramidal layer of the cornu ammonis 3 (CA3) and the subgranular zone of the dentate gyrus of the hippocampus. Moreover, MJ decreased the population of dead neuronal cells of the pyramidal layer of the CA3 and the subgranular zone of the dentate gyrus of the UCMS-mice, which suggests neuroprotection.
Taken together, these findings suggest that MJ demonstrated adaptogenic-like activity in mice; which might be related to modulation of serum corticosterone levels, inhibition of oxidative stress and neuroprotection.
This present study was carried out to investigate the likely mechanisms by which methyl jasmonate (MJ), ‘an agent widely used in aromatherapy for neurological disorders, attenuates lipopolysaccharide (LPS)-induced memory deficits in mice.
Mice were given the intraperitoneal administration of LPS (250 μg/kg) alone or in combination with MJ (10–40 mg/kg), donepezil, DP (1 mg/kg), or vehicle for 7 successive days. Thereafter, memory was assessed using object recognition test (ORT). Acetylcholinesterase and myeloperoxidase activities were estimated in brain tissue homogenates. Brain levels of nitric oxide and markers of oxidative stress, as well as histopathologic changes in the prefrontal cortex and cornu ammonis 1 (CA1) of the hippocampal region, were also assessed.
MJ (10–40 mg/kg) attenuated LPS-induced memory impairment in ORT. Moreover, the increased brain activities of Acetylcholinesterase and myeloperoxidase enzymes were suppressed by MJ when compared with control (p < 0.05). Increased brain oxidative stress and nitric oxide levels in LPS-treated mice were significantly decreased by MJ. It offers protection against LPS-induced neuronal degeneration of the prefrontal cortex and CA1 of the hippocampus, suggesting a neuroprotective effect.
Taken together, these findings showed that MJ offers protection against LPS-induced memory deficits via mechanisms related to inhibition of acetylcholinesterase, myeloperoxidase, oxidative stress and neuronal degeneration.
