Protective effects of myricetin on airway inflammation and oxidative stress in ovalbumin-induced asthma mice.
The Journal of nutritional biochemistry
Myricetin, a flavonoid isolated from many edible vegetables and fruits, has multiple biological effects, including anti-inflammatory and anti-tumor effects. Myricetin could inhibit mast cell degranulation in vitro, and it reduced the eosinophil content in bronchoalveolar lavage fluid (BALF) of ovalbumin (OVA)-sensitized mice. However, it remains unclear whether myricetin alleviates airway hyperresponsiveness (AHR), airway inflammation, and oxidative stress in asthma. Here, we investigated whether myricetin attenuated AHR, airway inflammation, and eosinophil infiltration in lungs of asthmatic mice. Mice were sensitized with OVA, then injected intraperitoneally with myricetin to investigate anti-inflammatory and antioxidant effects of myricetin. Moreover, we examined its effects on human bronchial epithelial BEAS-2B cells stimulated with TNF-α and IL-4, in vitro. Myricetin effectively mitigated eosinophil infiltration, AHR, and goblet cell hyperplasia in lung, and it reduced Th2 cytokine expression in BALF from asthmatic mice. Myricetin effectively promoted glutathione and superoxide dismutase productions and mitigated malondialdehyde expressions in mice by promoting Nrf2/HO-1 expression. Myricetin also reduced the production of proinflammatory cytokines, eotaxins, and reactive oxygen species in BEAS-2B cells. Myricetin effectively suppressed ICAM-1 expression in inflammatory BEAS-2B cells, which suppressed monocyte cell adherence. These results suggested that myricetin could effectively improve asthma symptoms, mainly through blocking Th2-cell activation, which reduced oxidative stress, AHR, and airway inflammation.
10.1016/j.jnutbio.2023.109485
Myricetin improves endurance capacity and mitochondrial density by activating SIRT1 and PGC-1α.
Scientific reports
Robust mitochondrial respiration provides energy to support physical performance and physiological well-being, whereas mitochondrial malfunction is associated with various pathologies and reduced longevity. In the current study, we tested whether myricetin, a natural flavonol with diverse biological activities, may impact mitochondrial function and longevity. The mice were orally administered myricetin (50 mg/kg/day) for 3 weeks. Myricetin significantly potentiated aerobic capacity in mice, as evidenced by their increased running time and distance. The elevated mitochondrial function was associated with induction of genes for oxidative phosphorylation and mitochondrial biogenesis in metabolically active tissues. Importantly, myricetin treatment led to decreased PGC-1α acetylation through SIRT1 activation. Furthermore, myricetin significantly improved the healthspan and lifespan of wild-type, but not Sir-2.1-deficient, C. elegans. These results demonstrate that myricetin enhances mitochondrial activity, possibly by activating PGC-1α and SIRT1, to improve physical endurance, strongly suggesting myricetin as a mitochondria-activating agent.
10.1038/s41598-017-05303-2
Unveiling myricetin's pharmacological potency: A comprehensive exploration of the molecular pathways with special focus on PI3K/AKT and Nrf2 signaling.
Journal of biochemical and molecular toxicology
Myricetin can be found in the traditional Chinese medicinal plant, Myrica rubra. Myricetin is a flavonoid that is present in many vegetables, fruits, and plants and is considered to have strong antioxidant properties as well as a wide range of therapeutic applications. Growing interest has been piqued by its classification as a polyphenolic molecule because of its potential therapeutic benefits in both the prevention and management of numerous medical conditions. To clarify myricetin's traditional medical uses, modern research has investigated various pharmacological effects such as antioxidant, anticancer, anti-inflammation, antiviral, antidiabetic, immunomodulation, and antineurodegenerative effects. Myricetin shows promise as a nutritional flavonol that could be beneficial in the prevention and mitigation of prevalent health conditions like diabetes, cognitive decline, and various types of cancer in humans. The findings included in this study indicate that myricetin has a great deal of promise for application in the formulation of medicinal products and nutritional supplements since it affects several enzyme activities and alters inflammatory markers. However, comprehensive preclinical studies and research studies are necessary to lay the groundwork for assessing myricetin's possible effectiveness in treating these long-term ailments. This review summarizes both in vivo and in vitro studies investigating myricetin's possible interactions through the nuclear factor-E2-related factor 2 (Nrf2) as well as PI3K (phosphatidylinositol 3-kinase)/AKT (protein kinase B) signaling pathways in an attempt to clarify the compound's possible clinical applicability across a range of disorders.
10.1002/jbt.23739
Myricetin improves apoptosis after ischemic stroke via inhibiting MAPK-ERK pathway.
Molecular biology reports
BACKGROUND:Neuronal apoptosis is the main cause for the disabilities and deaths of patients suffered with stroke. Neuroprotectants are clinically used to reduce neuronal apoptosis in ischemic stroke. However, the current neuroprotectants have multiple limitations. Myricetin is beneficial for multiple neurodegenerative diseases, but the role of myricetin as a neuroprotective agent in ischemic stroke is still not fully understood. METHODS AND RESULTS:Middle cerebral artery occlusion, Terminal deoxynucleotidyl transferase dUTP nick-end labeling staining and Western blots were used to explore the anti-apoptotic effects of myricetin in vivo. Flow cytometry, Western blots and Ca staining were used to study the neuroprotective effects of myricetin in vitro. In this study, we first demonstrated that myricetin reduced neuronal apoptosis after ischemia in vivo and in vitro. And, among the factors of apoptosis after ischemic stroke, excitotoxicity, oxidative stress and inflammation-induced apoptosis can be alleviated by myricetin. Moreover, we further demonstrated that myricetin was able to improve neuronal intrinsic apoptosis by inhibiting the phosphorylation of extracellular signal-regulated kinase in the oxygen and glucose deprivation in vitro. CONCLUSIONS:Summarily, our results support myricetin as a novel neuroprotectant for the prevention or treatment of ischemic stroke via MAPK-ERK signaling pathway.
10.1007/s11033-022-08238-8
Myricetin alleviates H2O2-induced senescence and apoptosis in rat nucleus pulposus-derived mesenchymal stem cells.
Folia histochemica et cytobiologica
INTRODUCTION:Transplantation of mesenchymal stem cells (MSCs) has been reported to be a novel promising target for the regeneration of degenerated intervertebral discs (IVDs). However, the culture and survival limitations of MSCs remain challenging for MSC-based biological therapy. Myricetin, a common natural flavonoid, has been suggested to possess antiaging and antioxidant abilities. Therefore, we investigated the biological function of myricetin, and its related mechanisms involving cell senescence in intervertebral disc degeneration (IDD). MATERIAL AND METHODS:The nucleus pulposus-derived mesenchymal stem cells (NPMSCs) were isolated from 4-month-old Sprague-Dawley (SD) rats and identified by examining surface markers and multipotent differentiation. Rat NPMSCs were cultured in an MSC culture medium or culture medium with different concentrations of H2O2. Myricetin or the combination of myricetin and EX527 were added to the culture medium to investigate the effects of myricetin. Cell viability was evaluated by cell counting kit-8 assays (CCK-8). The apoptosis rate was determined using Annexin V/PI dual staining. The mitochondrial membrane potential (MMP) was analyzed by a fluorescence microscope after JC-1 staining. The cell senescence was determined by SA-β-Gal staining. MitoSOX green was used to selectively estimate mitochondrial reactive oxygen species (ROS) Apoptosis-associated proteins (Bax, Bcl2, and cleaved caspase-3), senescence markers (p16, p21, and p53), and SIRT1/PGC-1α signaling pathway-related proteins (SIRT1 and PGC-1α) were evaluated by western blotting. RESULTS:The cells isolated from nucleus pulposus (NP) tissues met the criteria for MSCs. Myricetin showed no cytotoxicity up to a concentration of 100 μM in rat NPMSCs cultured for 24 h. Myricetin pretreatment exhibited protective effects against H₂O₂-induced apoptosis. Myricetin could also alleviate H₂O₂-induced mitochondrial dysfunctions of increased mitochondrial ROS production and reduced MMP. Moreover, myricetin pretreatment delayed rat NPMSC senescence, as evidenced by decreased exppression of senescence indicators. Pretreatment of NPMSCs with 10 μM EX527, a selective inhibitor of SIRT1, prior to exposure to 100 μM H2O2, reversed the inhibitory effects of myricetin on cell apoptosis. CONCLUSIONS:Myricetin could affect the SIRT1/PGC-1α pathway to protect mitochondrial functions and alleviate cell senescence in H₂O₂-treated NPMSCs.
10.5603/FHC.a2023.0007
Current Pharmacological Trends on Myricetin.
Gupta Gudiya,Siddiqui Mohd Aftab,Khan Mohd Muazzam,Ajmal Mohd,Ahsan Rabiya,Rahaman Md Azizur,Ahmad Md Afroz,Arshad Md,Khushtar Mohammad
Drug research
Myricetin is a member of the group of flavonoids called flavonols. Myricetin is obtained from various fruit, vegetables, tea, berries and red wine. Myricetin is characterized by the pysrogallol B-ring, and the more hydroxylated structure is known to be capable for its increased biological properties compared with other flavonols. Myricetin is produced by the Myricaceae, Anacardiaceae, Polygonaceae, Pinaceae and Primulacea families. It is soluble in organic solvent such as ethanol, DMSO (dimethyl sulfoxide), and dimethyl formamide (DMF). It is sparingly soluble in aqueous buffers. Myricetin shows its various pharmacological activities including antioxidant, anti-amyloidogenic, antibacterial, antiviral, antidiabetic, anticancer, anti-inflammatory, anti-epileptic and anti-ulcer. This review article focuses on pharmacological effects of Myricetin on different diseases such as osteoporotic disorder, anti-inflammatory disorder, alzheimer's disease, anti-epileptic, cancer, cardiac disorder, diabetic metabolic disorder, hepatoprotective disorder and gastro protective disorder.
10.1055/a-1224-3625
Myricetin: A review of the most recent research.
Song Xiaominting,Tan Lu,Wang Miao,Ren Chaoxiang,Guo Chuanjie,Yang Bo,Ren Yali,Cao Zhixing,Li Yuzhi,Pei Jin
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
Myricetin(MYR) is a flavonoid compound widely found in many natural plants including bayberry. So far, MYR has been proven to have multiple biological functions and it is a natural compound with promising research and development prospects. This review comprehensively retrieved and collected the latest pharmacological abstracts on MYR, and discussed the potential molecular mechanisms of its effects. The results of our review indicated that MYR has a therapeutic effect on many diseases, including tumors of different types, inflammatory diseases, atherosclerosis, thrombosis, cerebral ischemia, diabetes, Alzheimer's disease and pathogenic microbial infections. Furthermore, it regulates the expression of Hippo, MAPK, GSK-3β, PI3K/AKT/mTOR, STAT3, TLR, IκB/NF-κB, Nrf2/HO-1, ACE, eNOS / NO, AChE and BrdU/NeuN. MYR also enhances the immunomodulatory functions, suppresses cytokine storms, improves cardiac dysfunction, possesses an antiviral potential, can be used as an adjuvant treatment against cancer, cardiovascular injury and nervous system diseases, and it may be a potential drug against COVID-19 and other viral infections. Generally, this article provides a theoretical basis for the clinical application of MYR and a reference for its further use.
10.1016/j.biopha.2020.111017