\nIn the following lines you will be able to see how this substance, so present in our daily lives, would have impressive functions to reverse the aging of our cells, so that they remain active and functional for longer.
\nHere we start. <\/p>\n<\/p>\n
Aging <\/h1>\n
We have already talked a lot about the subject of aging and its different theories<\/a>, but today we will focus on fisetin as a molecule representing an active ingredient. According to recent findings, cellular senescence, which is essentially permanent, appears to play distinct roles in normal physiology and in various pathologies<\/strong>. If we remember the theory, aging is a highly malleable process that can be modulated in different ways, such as with calorie restriction, intermittent fasting, exercise, and a plant-based diet rich in phytochemicals<\/strong>. Fisetin (3,3\u2032,4\u2032,7-tetrahydroxyflavone) is a flavonol that has been identified as a secondary metabolite of many plants, found in their green parts, fruits, as well as bark and wood. Diet-derived antioxidants are increasingly being investigated for their health-promoting effects, including their role in cancer chemoprevention. Fisetin is currently being studied as one of the plant components of the diet and its role as an important epigenetic modulator of health status. The reason for this interest arises from relatively recent observations that fisetin is not only particularly effective as an antioxidant agent, but also shows remarkable selectivity in influencing multiple biological processes considered crucial for biological homeostasis<\/strong>.<\/p>\n In addition to antibiotic activity, fisetin shares distinct antioxidant activity with many other polyphenolic compounds, which was confirmed by several in vitro<\/em> and in vivo<\/em> models. Other activities along these lines include improving long-term memory, antidepressant effects, inhibition of ischemic reperfusion injury, and improvement of behavioral deficits after stroke.<\/p>\n<\/p>\n The chemistry of simple phenolics is quite complicated, and involves the reactivity of free radicals, ionoradicals, and organic ionic structures resulting from proton transfer. It has recently been shown that this natural compound could modulate different pleiotropic pathways (phosphatidylinositol-3-kinase\/protein kinase B\/mammalian target of rapamycin (PI3K\/Akt\/mTOR) and p38, mitogen-activated protein kinases (MAPK)-dependent kappalight factor-activated B-cell chain enhancer (NF-\u03baB)) that exerts a large number of biological effects including anti-inflammatory effects, hypolipidemic, hypoglycemic, antioxidant, neuroprotective, antiangiogenic and antitumor. https:\/\/doi.org\/10.1016\/j.ejphar.2021.174492<\/a><\/p>\n<\/p>\n It is becoming increasingly clear that neurological diseases are multifactorial and involve alterations in multiple cellular systems. Not only does fisetin have direct antioxidant activity, but it can also increase intracellular levels of glutathione, the main intracellular antioxidant. In the study that we will present below, we attempted to evaluate the potential role of fisetin as a caloric restriction mimetic for neuroprotection in models of natural and accelerated aging induced by D-galactose in rats. The data showed that fisetin significantly decreased the level of pro-oxidants and increased the level of antioxidants.<\/strong> In addition, it also improved mitochondrial membrane depolarization, apoptotic cell death, and alterations in synaptosome-bound ion transporter activities in the brains of aged rats. The accumulation of reactive oxygen species (ROS) due to age-related functional decline in mitochondria is most pronounced in energy-intensive tissues, such as skeletal muscle, the heart, and the brain. To determine radical scavenging activity, one study measured the percentage of 2,2-diphenyl-1-picrylhydracil (DPPH) radical inhibition with different concentrations of fisetin. There was a dose-dependent increase in the radical scavenging activity of fisetin.<\/strong> The percentage of DPPH radical inhibition was only 11.1 \u00b1 0.52% for 0.001 g\/l fisetin. Not only does fisetin have direct antioxidant activity but it can also increase intracellular levels of glutathione, the main intracellular antioxidant<\/strong>. Glutathione plays a central role in maintaining cellular redox homeostasis. How does fisetin maintain glutathione levels?
\nAlmost six decades ago, the phenomenon of the finite proliferation capacity of human fibroblasts was discovered (Hayflick, 1965<\/a>), initiating a period of extensive studies on the mechanisms of cell growth arrest, particularly in relation to the causes of the aging process. <\/p>\n
\nSenescent cell phenotypes, which normally secrete pro-inflammatory proteins and target apoptosis, can undergo certain modes of pharmacologically induced intervention that lead to the reversal of cellular fate. <\/p>\n
\nThe use of bioactive compounds to eliminate senescent cells has recently emerged as a promising approach to slow aging and reduce the severity of chronic diseases. <\/p>\n<\/p>\n What is fisetin?<\/h1>\n
\nThis substance shares distinct antioxidant properties with a host of other plant polyphenols<\/strong>.
\nIn addition, it exhibits a specific biological activity of considerable interest in terms of the protection of functional macromolecules against oxidative stress.
\nOn the other hand, it shows potential as an anti-inflammatory, chemopreventive, chemotherapeutic and recently also senotherapeutic agent.
\nDOI: 10.1017\/jns.2016.41<\/a> <\/p>\n
\nIn general, plant-based antioxidants have received a lot of attention, as they can be consumed for longer periods of time with very little or almost no adverse effects.
\nFlavonoids are a widely distributed class of plant pigments, which are regularly consumed in the human diet due to their abundance. <\/p>\n
\nThis substance is present in natural food products, distributed as follows: strawberries (Fragaria sp. 160 \u03bcg\/g), apples (Malus sp. 26.9 \u03bcg\/g), persimmons (Diospyros sp. 10.6 \u03bcg\/g), lotus roots (Nelumbo sp. 5.8 \u03bcg\/g), onions (Allium sp. 4.8 \u03bcg\/g), grapes (Vitis sp. 3.9 \u03bcg\/g), kiwis (Actinidia sp. 2.0 \u03bcg\/g), peaches (Prunus sp. 0.6 \u03bcg\/g), cucumbers (Cucumis sp. 0.1 \u03bcg\/g) and tomatoes (Solanum sp. 0.1 \u03bcg\/g). The average daily human intake is estimated to be around 0.4 mg.<\/strong> https:\/\/doi.org\/10.1016\/j.lfs.2017.12.005<\/a><\/p>\n
\nIn addition, antioxidant effects, and in particular the induction of glutathione synthesis, are considered important when it comes to neuroprotection. https:\/\/doi.org\/10.1089\/ars.2012.4901<\/a><\/p>\n How does it work?<\/h1>\n
\nPolyphenolic structures extended by the inclusion of a catechol ring are particularly susceptible to specific aromatic electron delocalization that may involve, as a result of contact with hydrogen acceptors, neighborhood quinone and diketone structures. https:\/\/doi.org\/10.1080\/10408390701856223<\/a><\/p>\n Neurological diseases<\/h2>\n
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\nThus, while each disease has its own mechanisms and pathologies of initiation, certain common pathways appear to be involved in most, if not all, diseases of this type.
\nTherefore, modulating a single factor is unlikely to be effective in preventing the development of the disease or slowing its progression. A better approach is to identify small molecules (<900 Daltons) that have multiple biological activities relevant to the maintenance of brain function. <\/strong><\/p>\n
\nIt can also activate key neurotrophic factor signaling pathways, has anti-inflammatory activity, and inhibits lipoxygenase activity, thereby reducing the production of pro-inflammatory eicosanoids and their byproducts. https:\/\/doi.org\/10.2741\/S425<\/a><\/p>\n
\nTo this end, young aged rats were supplemented for six weeks with 15 mg\/kg body weight of fisetin for the study with D-gal 500 mg\/kg body weight subcutaneously and also naturally aged rats.
\nA reverse transcription polymerase chain reaction (RT-PCR) gene expression analysis was performed to assess the expression of autophagy, neuronal, aging, and inflammatory marker genes.
\nApoptotic cell death and synaptosome membrane-bound ion transporter activities in brain tissues were also evaluated. <\/p>\n
\nRT-PCR data revealed that fisetin upregulated the expression of autophagy genes (Atg-3 and Beclin-1), sirtuin-1, and neuronal markers (NSE and Ngb), and negatively regulated the expression of inflammatory genes (IL-1\u03b2 and TNF-\u03b1 genes) and Sirt-2 respectively in the aging brain. https:\/\/doi.org\/10.1016\/j.lfs.2017.11.004<\/a><\/p>\n<\/p>\n Action on the mitochondria<\/h2>\n
\nAge-related increase in ROS plays an essential role in myocyte apoptosis in the aging heart and the development of cardiovascular diseases, including atherosclerosis.
\nEmerging evidence suggests that ROS-induced oxidative damage contributes to brain aging.
\nThe death of neuronal and glial cells is a major cause of brain aging.
\nElevated ROS levels also correlate with an increase in age-related neuroinflammation, which can lead to neurodegeneration. <\/p>\n
\nHowever, the inhibition effect increased to 76.9 \u00b1 0.37% for 0.1 g\/L fisetin and 89.0 \u00b1 0.57% for 2 g\/L fisetin.
\nIn addition to the radical scavenging activity in vitro, the effect of fisetin on cellular ROS levels in vivo was examined, which decreased significantly in the treated animals compared to the control. https:\/\/doi.org\/10.3390\/ph15121528<\/a><\/p>\n<\/p>\n Effects on intracellular glutathione<\/h2>\n
\nThe compound may also maintain mitochondrial function in the presence of oxidative stress.
\nIn addition, it has anti-inflammatory activity against microglial cells and inhibits the activity of 5-lipoxygenase, thus reducing the production of lipid peroxides and their pro-inflammatory byproducts. <\/p>\n
\nA fairly significant number of studies have demonstrated age-dependent decreases in total glutathione. The age-related declines seen in many studies could be due to increased consumption, decreased production, or a combination of both.<\/strong> Higher consumption would be consistent with an increase in ROS production with age.
\nHowever, recent studies suggest that decreased production also plays an important role in the decline of brain GSH with age. <\/p>\n
\nIn general, intracellular levels are regulated by a complex series of mechanisms including substrate availability and transport, synthesis and regeneration rates, glutathione utilization, and outflow to extracellular compartments.
\nBecause glutamate and glycine are found in relatively high intracellular concentrations, cysteine limits glutathione synthesis in many cell types, including nerve cells.
\nIn the extracellular environment, cysteine is readily oxidized to form cystine, so for most cell types, cystine transport mechanisms are essential to provide them with the cysteine needed for glutathione synthesis. https:\/\/doi.org\/10.1007\/s12263-009-0142-5<\/a><\/p>\n<\/p>\n ACTIVATE REVIVE CELL PHONE<\/h1>\n
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