Naringenin protects against oxido-inflammatory aberrations and altered tryptophan metabolism in olfactory bulbectomized-mice model of depression

Bansal, Yashika; Singh, Raghunath; Saroj, Priyanka; Sodhi, Rupinder Kaur; Kuhad, Anurag

doi:10.1016/j.taap.2018.07.010

Cited by 66 publications

(25 citation statements)

References 73 publications

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“…Neither Ket nor GUO affected the hyperactivity induced by OBX, a hallmark of the OBX behavioral phenotype 9,53 . Magnetic resonance studies showed that OBX leads to gross structural changes in rodent brain including significant amygdala impairment 54,55 . The amygdala, involved in the emotional salience of environmental stimuli and modulation of affective states 56 , seems to be key for OBX hyperactivity.…”

Section: Discussionmentioning

confidence: 99%

Guanosine fast onset antidepressant-like effects in the olfactory bulbectomy mice model

Almeida

Pocharski

Rodrigues

et al. 2020

Sci Rep

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The treatment of major depressive disorder (MDD) is still a challenge. In the search for novel antidepressants, glutamatergic neuromodulators have been investigated as possible fast-acting antidepressants. Innovative studies suggest that the purine cycle and/or the purinergic signaling can be dysregulated in MDD, and the endogenous nucleoside guanosine has gained attention due to its extracellular effects. This study aimed to verify if guanosine produces fast-onset effects in the wellvalidated, reliable and sensitive olfactory bulbectomy (OBX) model of depression. The involvement of the mTOR pathway, a key target for the fast-onset effect of ketamine, was also investigated. Results show that a single i.p. injection of guanosine, or ketamine, completely reversed the OBX-induced anhedonic-like behavior 24 or 48 h post treatment, as well as the short-term recognition memory impairment 48 h post treatment. The antidepressant-like effects of guanosine and ketamine were completely abolished by rapamycin. This study shows, for the first time, that guanosine, in a way similar to ketamine, is able to elicit a fast antidepressant response in the OBX model in mice. The results support the notion that guanosine represents a new road for therapeutic improvement in MDD. Major depressive disorder (MDD), a severe psychiatric condition, is characterized by high prevalence 1 and disability for affected individuals 2,3 , leading to elevated economic burden 1,4 and a substantial percentage (circa 30%) of patients unresponsive to treatment 4,5. Though this picture vindicates the search for superior medication 6 , unfortunately most research results has been limited to more drugs with the same mechanism of action, or at best certain incremental innovation 7,8. A major flaw in treating depression is the time lag between the onset of the treatment and the remission of the symptoms 4. Especially relevant for treating patients is skepticism, this delay obstructs adhesion, prolongs suffering and disability, and increase suicide risk 4,9. Ketamine has emerged as a fast-acting antidepressant agent that is effective to elicit rapid effect even for severe depressed patients refractory to antidepressant treatment 10. However, ketamine seems to be an unsecure drug especially under repeated administration. This limitation of ketamine's use has lead to renewed efforts for pursuing novel fast-acting antidepressant agents, especially glutamatergic neuromodulators, including guanosine (GUO) 9,11-13. Several lines of evidence suggest that the purine cycle and/or the purinergic signaling could be dysregulated in MDD patients 14-17. As purinergic signaling modulate cell proliferation, differentiation, neuron-glia crosstalk, and inflammation 17-19 , disturbances in purine homeostasis contribute to the pathophysiological process underlying MDD 15,18. GUO is an endogenous nucleoside with neuroprotective effects shown in different animal models of brain disorders 17,20,21. In conditions under which brain homeostasis is disrupted GUO seems to play an importa...

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Section: Discussionmentioning

confidence: 99%

Guanosine fast onset antidepressant-like effects in the olfactory bulbectomy mice model

Almeida

Pocharski

Rodrigues

et al. 2020

Sci Rep

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“…Examples of this include 2,3,5,4'-tetrahydroxystilbene-2-O-β-D-glucopyranoside [248] and vorinostat [249], which ameliorate inflammatory damage and OS to exert the antidepressant effect. Moreover, naringenin [250,251], iptakalim [252], silymarin [253], resveratrol [254], honokiol [255], ketamine [256], melatonin [257], oxytocin [258], vanillin [259], trigonelline [260] , quercetin [261], αtocopherol [262], baicalin [263] and selenium-containing compounds [264] have neuroprotective effects in the hippocampus of mice due to their antioxidant and antiinflammatory properties. Particularly, ketamine is involved in inducing the rapid antidepressant effects through increasing the release of glutamate in the body [265] and affecting energy metabolism in MDD [256].…”

Section: Antioxidants In Depressionmentioning

confidence: 99%

Oxidative Stress at the Crossroads of Aging, Stroke and Depression

et al. 2020

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Epidemiologic studies have shown that in the aging society, a person dies from stroke every 3 minutes and 42 seconds, and vast numbers of people experience depression around the globe. The high prevalence and disability rates of stroke and depression introduce enormous challenges to public health. Accumulating evidence reveals that stroke is tightly associated with depression, and both diseases are linked to oxidative stress (OS). This review summarizes the mechanisms of OS and OS-mediated pathological processes, such as inflammation, apoptosis, and the microbial-gut-brain axis in stroke and depression. Pathological changes can lead to neuronal cell death, neurological deficits, and brain injury through DNA damage and the oxidation of lipids and proteins, which exacerbate the development of these two disorders. Additionally, aging accelerates the progression of stroke and depression by overactive OS and reduced antioxidant defenses. This review also discusses the efficacy and safety of several antioxidants and antidepressants in stroke and depression. Herein, we propose a crosstalk between OS, aging, stroke, and depression, and provide potential therapeutic strategies for the treatment of stroke and depression.

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“…The flavonoid Naringenin functions as antidepressant by restoring serotonin and noradrenaline levels in brain tissue [99]. In bulbectomized mice, two weeks of Naringenin treatment ameliorated depression like behavioral alterations, decreased elevated pro-inflammatory cytokines and increased levels of BDNF and serotonin in hippocampus and cortex [100].…”

Section: Drugsmentioning

confidence: 99%

Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction

Bhatia‐Dey¹,

Heinbockel²

2020

Sino-Nasal and Olfactory System Disorders [Working Title]

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Olfaction is an underestimated sensory modality in terms of its predictive value as an indicator of disorders. It is a well-known phenomenon that a significant percentage of people afflicted with certain prevalent disorders causing degenerative neuropathology, progressive loss of memory and communication function, normal age-based decline of physiological functions, intellectual challenges, depressive and anxiety disorders as well as post-traumatic stress disorders, present with a range of olfactory deficits. Here, we review our understanding of these deficits and their relation to various clinical manifestations such as neurological and neuropsychiatric diseases and disorders. At the outset, we will briefly describe the olfactory pathway from olfactory sensory neurons in the nasal epithelium to the olfactory bulb and on to olfactory cortical and subcortical structures involved in olfaction such as the amygdala.

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Naringenin protects against oxido-inflammatory aberrations and altered tryptophan metabolism in olfactory bulbectomized-mice model of depression

Cited by 66 publications

References 73 publications

Guanosine fast onset antidepressant-like effects in the olfactory bulbectomy mice model

Guanosine fast onset antidepressant-like effects in the olfactory bulbectomy mice model

Oxidative Stress at the Crossroads of Aging, Stroke and Depression

Neurological and Neuropsychiatric Disorders in Relation to Olfactory Dysfunction

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