Probable mechanisms involved in the antipsychotic-like activity of morin in mice

Ben‐Azu, Benneth; Aderibigbe, Adegbuyi Oladele; Omogbiya, Itivere Adrian; Ajayi, Abayomi Mayowa; Owoeye, Olatunde; Olonode, Elizabeth Toyin; Iwalewa, Ezekiel O.

doi:10.1016/j.biopha.2018.06.057

Cited by 61 publications

(40 citation statements)

References 59 publications

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“…However, NOS inhibitors increased the concentration of 5‐HT in the hippocampus freely moving rats (Wegener, Volke, & Rosenberg, ) and in the forced swim test (Harkin et al, ; Ulak et al, ). Earlier on, we reported that morin attenuated alterations in 5‐HTergic transmission in socially impaired mice brains (Ben‐Azu, Aderibigbe, Omogbiya, et al, ). In this study, it was found that the antidepressant‐like activity of morin was abolished by pretreatment with l ‐arginine, suggesting the role of NO in the antidepressant action of morin.…”

Section: Discussionmentioning

confidence: 87%

“…More importantly, different studies have tried to unmask specific mechanisms of action of morin on different neuropsychiatric disease conditions. For example, morin has been shown to attenuate different neurochemical changes and decreased oxidative stress in brains of mice relevant to the neuropsychiatric pathology of schizophrenia, behavioral despair (Ben‐Azu, Aderibigbe, Eneni, et al, ; Ben‐Azu et al, ), Parkinson's disease (Zhang et al, ) and Alzheimer's disease (Lemkul & Bevan, ). Morin also decreases loss of cortical pyramidal via inhibition of neuroinflammation and nitrergic stress in a two‐hit mouse model of schizophrenia (Ben‐Azu et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of l‐arginine‐nitric oxide pathway in the antidepressant and memory promoting effects of morin in mice

Ben‐Azu

Aderibigbe

Ajayi

et al. 2019

Drug Development Research

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l‐Arginine‐nitric oxide pathway has been reported to be involved in the mediation of the psychopharmacological effects of many psychotropic drugs. Previous studies have shown that morin, a psychotropic compound isolated from mulberry leaf produces functional psychopharmacological effects indicative of antidepressant, antipsychotic, anxiolytic and nootropic properties. However, the role of l‐arginine‐nitric oxide pathway in the psychotropic effects of morin has not been fully investigated, hence, the need for this study. Male Swiss mice were pretreated individually or in combination with nitric oxide precursor [l‐arginine (750 mg/kg, i.p.)], competitive nonselective nitric oxide synthase (NOS) inhibitor [N(G)‐nitro‐l‐arginine methyl ester (l‐NAME, i.p) (50 mg/kg)] or selective neuronal NOS inhibitor [methylene blue (3.75 mg/kg, i.p)] prior to morin (100 mg/kg, i.p.) or saline (10 mL/kg, i.p.) treatment. Psychopharmacological activities were then evaluated 30 min later using open field, Y‐maze, and forced swim tests. l‐Arginine significantly reversed the effects of morin on locomotion, memory and depression in mice. The reduced motor activity and enhanced memory function produced by morin were significantly attenuated by methylene blue but augmented the antimobility activity of morin in the FST. Moreover, l‐NAME potentiated the psychopharmacological effects of morin in the open field and forced swim tests but reduced its memory promoting effect. Meanwhile, morin supplementation reversed the effects of l‐arginine on l‐NAME‐treated mice in all behavioral models. The results of this study suggest that l‐arginine‐nitric oxide pathway might play a role in the modulation of the antidepressant and memory promoting effects of morin in mice.

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Section: Discussionmentioning

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Involvement of l‐arginine‐nitric oxide pathway in the antidepressant and memory promoting effects of morin in mice

Ben‐Azu

Aderibigbe

Ajayi

et al. 2019

Drug Development Research

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“…Consequently, previous studies have demonstrated that underfeeding during pregnancy resulted in growth retardation and a delayed onset of puberty ( Engelbregt et al., 2000 ). Although earlier studies have proposed that more than weight, an appropriate body composition or a certain percentage of fat is needed to start puberty in rats ( Bouret et al., 2004 ; Frisch & Revelle, 1971 ). Therefore, it is plausible to speculate that a low percentage of fat or low birth weight might delay the onset of certain developmental features including puberty and neurocognitive functions ( Bouret et al., 2004 ; Frisch & Revelle, 1971 ).…”

Section: Discussionmentioning

confidence: 99%

“…Consequently, early malnutrition is known to change the original programming of organs, especially during developmental phases, which can result in long term metabolic changes in weight and growth patterns, as well as feeding behavior ( Engelbregt et al., 2000 ; Engelbregt et al., 2001 ). It is well-known that metabolic adaptations to under-nutrition are linked to changes in endocrine microenvironments as well as orexigenic and anorexigenic hormones ( Gualillo et al., 2012 ; Bouret et al., 2004 ). Ghrelin, which is an orexigenic hormone primarily expressed in the stomach and hypothalamus, is one of the most researched gut-derived molecules and is an endogenous ligand for growth hormone secretagogues and food intake ( Gualillo et al., 2012 ; Rojas et al., 2011 ).…”

Section: Introductionmentioning

confidence: 99%

“…Mechanistically, peripheral ghrelin and leptin are known to enter into certain areas of the brain through the blood brain barrier to modulate cascade of events including signal transduction and activator of transcription-3 (STAT3) and MAPK pathways, from where they are known the regulate various “hunger and satiety centres” in the lateral hypothalamic area, arcuate and paraventricular nuclei ( Rojas et al., 2011 ; Hu et al., 2003 ; Sucajtys-Szulc et al., 2010 ). However, several studies have shown opposite correlations between human and animal ghrelin and leptin levels, feeding behavior, body mass and pubertal onset ( Gualillo et al., 2012 ; Bouret et al., 2004 ; Quennell et al., 2011 ). For a long time, it was hypothesized that ghrelin and leptin played important roles in the central regulation of body weight and thus, it has been reported that fasting or under-nutrition has significant implication in the pathophysiology of several metabolic diseases like growth hormone deficiencies, anorexia nerovosa, cachexia, gastrointestinal motility disorders and obesity ( Gualillo et al., 2012 ; Quennell et al., 2011 ; Cordido et al., 2009 ).…”

Section: Introductionmentioning

confidence: 99%

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Prenatal and early postnatal food restrictions cause changes in brain oxidative status and orexigenic/anorexigenic hormones in the offspring of rats: prevention by quercetin and kaempferol

Anachuna¹,

Moke²,

Iyare³

et al. 2020

Current Research in Pharmacology and Drug Discovery

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Brain oxidative signaling pathways have been identified as important targets for alleviating food deprivation-induced changes in metabolic gate-ways. Previous studies have shown that prenatal and early postnatal malnutrition alters leptin and ghrelin signaling via oxidative pathways. Thus, it has been hypothesized that agents with antioxidant properties might be beneficial for the mitigation of prenatal and early postnatal food scarcity-induced oxidative damage. Quercetin and kaempferol are natural bioflavonoids with proven antioxidant properties. In this study, we evaluated their effects on prenatal maternal food consumption, maternal and pup weights, biomarkers of orexigenic and anorexigenic hormones and oxidative stress in rats. Rats were allotted into different treatment groups (n = 6) in three different experiments (prenatal, postnatal food-deprivations or both). Prenatal-food restriction (PrNFR) was induced by 50% of ad libitum accessible diet during pregnancy till parturition and postnatal-food restriction (PsNFR) was simulated by litter-enlargement to 16 pups per mother from postnatal day (PND) 2. Rats in each experiment were concurrently treated with vehicle (10 mL/kg), quercetin (50, 100 and 200 mg/kg, p.o.) or kaempferol (50, 100 and 200 mg/kg, p.o.) respectively. A third experimental group consisted of both protocols. Quercetin and kaempferol dose-dependently increased the body weights of pups exposed to PrNFR, PsNFR and PrNFR-PsNFR at PNDs 1–22 respectively. Both compounds increased maternal body weights but attenuated maternal food-intake at prenatal days 7 and 14 due by PrNFR. Quercetin and kaempferol reduced brain malondialdehyde concentrations and increased glutathione levels in PrNFR, PsNFR and PrNFR-PsNFR-exposed offspring of rats. Importantly, quercetin and kaempferol significantly ( p < 0.05) prevented PrNFR-, PsNFR- or PrNFR-PsNFR-induced alterations in leptin and ghrelin levels. Cumulatively, quercetin and kaempferol increased pup and maternal weights and attenuated maternal food-intake of rats submitted to PrNFR, PsNFR and PrNFR-PsNFR respectively, likely via nutrigenomic modulations of orexigenic/anorexigenic hormones and inhibition of brain oxidative stress.

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Morin improves learning and memory in healthy adult mice

Martínez‐Coria,

Serrano‐García,

López‐Valdés

et al. 2024

Brain and Behavior

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BackgroundMorin is a flavonoid found in many edible fruits. The hippocampus and entorhinal cortex play crucial roles in memory formation and consolidation. This study aimed to characterize the effect of morin on recognition and space memory in healthy C57BL/6 adult mice and explore the underlying molecular mechanism.MethodsMorin was administered i.p. at 1, 2.5, and 5 mg/kg/24 h for 10 days. The Morris water maze (MWM), novel object recognition, novel context recognition, and tasks were conducted 1 day after the last administration. The mice's brains underwent histological characterization, and their protein expression was examined using immunohistochemistry and Western blot techniques.ResultsIn the MWM and novel object recognition tests, mice treated with 1 mg/kg of morin exhibited a significant recognition index increase compared to the control group. Besides, they demonstrated faster memory acquisition during MWM training. Additionally, the expression of pro‐brain‐derived neurotrophic factor (BDNF), BDNF, and postsynaptic density protein 95 proteins in the hippocampus of treated mice showed a significant increase. In the entorhinal cortex, only the pro‐BDNF increased. Morin‐treated mice exhibited a significant increase in the hippocampus's number and length of dendrites.ConclusionThis study shows that morin improves recognition memory and spatial memory in healthy adult mice.

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Probable mechanisms involved in the antipsychotic-like activity of morin in mice

Cited by 61 publications

References 59 publications

Involvement of l‐arginine‐nitric oxide pathway in the antidepressant and memory promoting effects of morin in mice

Involvement of l‐arginine‐nitric oxide pathway in the antidepressant and memory promoting effects of morin in mice

Prenatal and early postnatal food restrictions cause changes in brain oxidative status and orexigenic/anorexigenic hormones in the offspring of rats: prevention by quercetin and kaempferol

Morin improves learning and memory in healthy adult mice

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