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30 Central Nervous System Agents in Medicinal Chemistry, 2013, 13, 30-35
Neuroprotective Actions of Flavones and Flavonols: Mechanisms and
Relationship to Flavonoid Structural Features
Federico Dajas
*
, Abin-Carriquiry Juan Andrés, Arredondo Florencia, Echeverry Carolina and
Rivera-Megret Felicia
Department of Neurochemistry, Instituto de Investigaciones Biológicas Clemente Estable, Montevideo, Uruguay
Abstract: Epidemiological studies have shown positive preventive action of flavonoids on cardiovascular and
neurodegenerative events. Among the six groups in which flavonoids are classified, the flavones and flavonols, based on
the backbone of 2-phenylchromen-4-one (2-phenyl-1-benzopyran-4-one) are the most commonly encountered within the
families and genera of the higher plants. Numerous studies support a neuroprotective activity of flavones such as luteolin
and flavonols such as kaempherol and quercetin in experimental focal ischemia and models of neurodegeneration.
Antioxidation, modulation of signaling cascades and gene expression as well as anti-inflammation appear as the main
protective mechanisms and mitochondria are a likely main target mediating the preventive actions against oxidative stress.
Flavones and flavonols re-establish the redox regulation of proteins, transcription factors and signaling cascades that are
otherwise inhibited by elevated oxidative stress. The final survival or death of the neuron depends on flavone and flavonol
concentrations, time of exposure and, mainly, metabolic and oxidative neuronal circumstances. Neuroprotection appears
to be linked to specific structural motifs, beyond those involved in antioxidation. By themselves or as templates for
synthetic compounds, flavone and flavonol molecules show potential as multi-targeted therapeutic tools for protecting the
brain. Nonetheless, more research needs to be done on the correlation of potential beneficial effects of flavones and
flavonols and their mechanisms of action.
Keywords: Flavones, flavonols, neuroprotection, oxidative stress, quercetin, signalling.
1. INTRODUCTION
1.1. Brain Pathology, Redox Homeostasis and Oxidative
Stress
It is known that brain pathology in the form of
cerebrovascular and neurodegenerative disease is a leading
cause of death all over the world, with an incidence of about
2/1000 and an 8% total death rate [1, 2]. Moreover, stroke
and dementia are a source of high individual and family
suffering mainly because of the lack of efficient therapeutic
alternatives. The latter motivates research efforts to identify
the mechanisms of neuronal death and to discover new
compounds to prevent them. Neuronal death in these
neuropathologies is a complex phenomenon involving failure
of metabolic processes, protein impaired mitochondrial
function, increased oxidative damage, defects in the
proteasome system, protein aggregation, changes in iron
metabolism, and events of excitotoxicity and inflammation
[3]. The interaction between all these cellular processes
would not be necessarily a cascade but a cycle of events, of
which oxidative stress is a major component [4].
Under physiologic conditions, the balance between the
generation and the elimination of reactive oxygen and
nitrogen species (ROS, NOS) maintains a redox homeostasis
*Address correspondence to this author at the Department of
Neurochemistry, Instituto de Investigaciones Biológicas Clemente Estable,
Avda Italia 3318, 11600, Montevideo, Uruguay; Tel:/Fax: 5982 4872603;
E-mail: fdajas@gmail.com
to ensure the correct function of redox-sensitive signaling
proteins. However, when homeostasis is disturbed, oxidative
stress may take place leading to damage of lipids, proteins
and nucleic acids and disruption of redox signaling [5, 6].
Aberrant redox cell signaling may in turn cause cell death,
contributing to disease onset [7-10].
With only 2% of the body weight, the brain represents
almost 20% of the O
2
consumption of the organism [11].
Indeed, because of its high metabolic rate and relatively
reduced capacity for cellular defense and regeneration
compared with other organs, the brain is believed to be
particularly susceptible to oxidative stress events. In this
sense, the maintenance of cellular redox homeostasis appears
as a cue to the control and the prevention of oxidative stress-
related brain diseases [12, 13].
The above-described situation has led to the search of a
variety of antioxidant approaches to attenuate acute ischemic
and chronic neurodegenerative disease injuries [14, 15].
Nevertheless, promising results showing strong neuroprotective
effects in different preclinical models, failed systematically
in clinical trials [16]. In this context, it is likely that
molecules acting on multiple targets and involved in all the
events of the neurodegenerative processes would be required
to be therapeutically effective [3].
1.2. Flavonoids: Flavones and Flavonols
Flavonoids represent the most common group of
polyphenolic compounds in the human diet and are widely
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