Hesperidin, a flavonoid glycoside with sedative effect, decreases brain pERK1/2 levels in mice

Martinez, Milka; Fernandez, Sebastian P.; Loscalzo, Leonardo M.; Wasowski, Cristina; Paladini, Alejandro C.; Marder, Mariel; Medina, Jorge H.; Viola, Haydeé

doi:10.1016/j.pbb.2008.12.016

Cited by 30 publications

(20 citation statements)

References 41 publications

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“…Our results corroborate other findings [13,16,42], that demonstrated that a similar flavonoid, hesperitin, affects the phosphorylation state of ERK 1/2 kinases, a member of MAPK pathway. In contrast, whereas those works demonstrated a distinction between the antioxidation and neuroprotection effects of hesperitin, our data suggest that activation of ERK1/2 and Akt might be linked to proposed that flavanones may protect neurons by activation of both ERK and Akt signalling pathways.…”

Section: Discussionsupporting

confidence: 92%

Hesperidin, a Flavone Glycoside, as Mediator of Neuronal Survival

2011

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Flavonoids comprise the most common group of plant polyphenols and provide much of the flavor and color to fruits and vegetables. More than 5,000 different flavonoids have been described. The biological activities of flavonoids cover a very broad spectrum, from anticancer and antibacterial activities to inhibition of bone reabsorption and neuroprotection effect. Although emerging evidence suggests that flavonoids have an important role on brain development, little is known about their mechanisms of action. In the present work, we performed a screening of flavonoid actions by analyzing the effects of these substances (hesperidin and rutin) on neural progenitors and neuronal morphogenesis in vitro. We demonstrated that treatment of neural progenitors with the flavonoid hesperidin enhanced neuronal population as revealed by an 80% increase in the number of β-tubulin III cells. This effect was mainly due to modulation of neuronal progenitor survival. Pools of astrocyte and oligodendrocyte progenitors were not affected by hesperidin whereas rutin had no effect on neuronal population. We also demonstrated that the flavonoid hesperidin modulates neuronal cell death by activating MAPK and PI3K pathways. This opens the possibility of using flavonoids for potential new therapeutic strategies for neurodegenerative diseases.

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Section: Discussionsupporting

confidence: 92%

Hesperidin, a Flavone Glycoside, as Mediator of Neuronal Survival

2011

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“…In addition, various studies showed that Hsd attenuates cell damage by augmenting cellular defenses. Hsd promoted or upregulated the gene expression of Nrf2 and ERK 1/2 (Elavarasan et al, 2012;Martinez et al, 2009). The activation of Nrf2 and ERK 1/2 led to the upregulation of HO-1 expression, resulting in a decrease in intracellular pro-oxidants and an increase in bilirubin as an internal antioxidant.…”

Section: Antioxidant Propertiesmentioning

confidence: 99%

Antioxidant and Anti-Inflammatory Properties of the Citrus Flavonoids Hesperidin and Hesperetin: An Updated Review of their Molecular Mechanisms and Experimental Models

et al. 2014

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Inflammation and oxidative stress are two major causes of various life-threatening diseases. Hesperidin (Hsd) and its aglycone, hesperetin (Hst), are two flavonoids from citrus species that have numerous biological properties, particularly antioxidant and anti-inflammatory. New findings showed that the antioxidant activity of Hsd/Hst was not only limited to its radical scavenging activity, but it augmented the antioxidant cellular defenses via the ERK/Nrf2 signaling pathway as well. Various in vitro and in vivo studies have been conducted to evaluate Hsd, its metabolites, or its synthetic derivatives at reducing inflammatory targets including NF-κB, iNOS, and COX-2, and the markers of chronic inflammation. In this review, new findings regarding the molecular targets of Hsd and Hst in the reduction of oxidative stress are discussed. Also, in the anti-inflammatory section, we provide a summary of significant investigations concerning the mechanisms of action based on the studied inflammation models.

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“…Oral treatment with HP (50 and 100 mg/kg) for two weeks was reported to elicit anxiolytic and locomotive-enhancing effects in immobilization-stressed mice (Viswanatha et al, 2012[45]). Nevertheless, HP has repeatedly found to exhibit a strong sedative impact in mice (Loscalzo et al, 2008[27]; Martínez et al, 2009[30]). Therefore, our findings suggest that the anxiolytic efficacy of HP can be hidden by its sedative repercussion as the treatment progresses, which is correlated with the evolving FA-related sickness behavior in pregnant rats.…”

Section: Discussionmentioning

confidence: 99%