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dihydromyricetin/възпаление
Линкът е запазен в клипборда
Страница 1 от 55 резултата
Dihydromyricetin is a new inhibitor of influenza polymerase PB2 subunit and influenza-induced inflammation
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Development of new and effective anti-influenza drugs is critical for the treatment of influenza virus infection. The polymerase basic 2 (PB2) subunit as a core subunit of influenza A virus RNA polymerase complex is considered to be an attractive drug target for anti-influenza drug discovery.
Semi-preparative separation of dihydromyricetin enantiomers by supercritical fluid chromatography and determination of anti-inflammatory activities.
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Dihydromyricetin, extracted from Ampelopsis grossedentata, has been widely used as one of Chinese health products in recent years. However, limited chiral separation method hinders the studies of pharmacological and pharmacokinetic activity differences of (+)-dihydromyricetin, (-)-dihydromyricetin,
Dihydromyricetin Inhibits Lead-Induced Cognitive Impairments and Inflammation by the Adenosine 5'-Monophosphate-Activated Protein Kinase Pathway in Mice.
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Dihydromyricetin (DHM), a natural flavonoid derived from the medicinal and edible plant Ampelopsis grossedentata, exhibits antioxidant, antiapoptosis, antitumor, and anti-inflammatory bioactivities. This study evaluated the effects of DHM on Pb-induced neurotoxicity and explored the underlying
Semaphoring 4D is required for the induction of antioxidant stress and anti-inflammatory effects of dihydromyricetin in colon cancer.
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Semaphorin 4D (Sema4D) has been involved in cancer progression, the expression of which is associated with the poor clinical outcomes of some cancer patients. Dihydromyricetin (DMY) has antitumor potentials for different types of human cancer cells. However, the pharmacological effects of DMY on
Dihydromyricetin improves glucose and lipid metabolism and exerts anti-inflammatory effects in nonalcoholic fatty liver disease: A randomized controlled trial.
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Ampelopsis grossedentata, a medicinal and edible plant, has been widely used in China for hundreds of years, and dihydromyricetin is the main active ingredient responsible for its various biological actions. We investigated the effects of dihydromyricetin on glucose and lipid metabolism,
Dihydromyricetin Inhibits Inflammation of Fibroblast-Like Synoviocytes through Regulation of Nuclear Factor-κB Signaling in Rats with Collagen-Induced Arthritis.
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Dihydromyricetin (DMY), the main flavonoid of Ampelopsis grossedentata, has potent anti-inflammatory activity. However, the effect of DMY on chronic autoimmune arthritis remains undefined. In this study, we investigated the therapeutic effects of DMY on collagen-induced arthritis (CIA).
Dihydromyricetin relieves rheumatoid arthritis symptoms and suppresses expression of pro-inflammatory cytokines via the activation of Nrf2 pathway in rheumatoid arthritis model.
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Rheumatoid arthritis (RA) is a systemic inflammatory and autoimmune disease. In this research, we estimated the protective effects of Dihydromyricetin (DMY) on RA induced by Complete Freund's Adjuvant (CFA). We found that DMY effectively relieved rheumatoid arthritis symptoms, such as body weight
Dihydromyricetin Attenuates Inflammation through TLR4/NF-kappaB Pathway.
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Microglia plays a complex role in neuroinflammation, which has been implicated in neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. This study aims to explore the effect and mechanism of Dihydromyricetin (DHM) on lipopolysaccharide (LPS)-induced inflammation in
Suppression of Inflammatory Responses by Dihydromyricetin, a Flavonoid from Ampelopsis grossedentata, via Inhibiting the Activation of NF-κB and MAPK Signaling Pathways.
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Ampelopsis grossedentata, an indigenous plant in southern China, has been used for treating pharyngitis in traditional Chinese medicine for hundreds of years. In this study, we explored the anti-inflammatory activity of dihydromyricetin (1), its major bioactive component, and the underlying
Anti‑inflammatory effects of dihydromyricetin in a mouse model of asthma.
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Dihydromyricetin (DHM) is a plant flavonoid and is the primary active ingredient isolated from the medicinal herb, Ampelopsis grossedentata. DHM has been shown to possess various pharmacological activities, including anti‑inflammatory effects. However, the possible role of DHM in asthma treatment
Dihydromyricetin suppresses inflammatory responses in vitro and in vivo through inhibition of IKKβ activity in macrophages.
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Dihydromyricetin (DMY) a flavonoid derived from medicinal plant Ampelopsis grossedentata, possesses anti-oxidative and anti-inflammatory effects in vitro, however, the in vivo anti-inflammatory action of DMY remains unknown. In the current study, carrageenan-induced paw edema in rat, an acute
Mutation of cysteine 46 in IKK-beta increases inflammatory responses.
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Activation of IκB kinase β (IKK-β) and nuclear factor (NF)-κB signaling contributes to cancer pathogenesis and inflammatory disease; therefore, the IKK-β-NF-κB signaling pathway is a potential therapeutic target. Current drug design strategies focus on blocking NF-κB signaling by binding to specific
Inhibitory effect of a flavonoid dihydromyricetin against Aβ40 amyloidogenesis and its associated cytotoxicity.
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Misfolding and fibrillogenesis of amyloid-β protein (Aβ) play a key role in the onset and progression of Alzheimer's disease (AD). Screening for inhibitors against Aβ amyloidogenesis is helpful for rational designing and developing new anti-AD drugs and therapeutic strategies. Dihydromyricetin, a
Dihydromyricetin improves vascular hyporesponsiveness in experimental sepsis via attenuating the over-excited MaxiK and KATP channels.
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BACKGROUND
Dihydromyricetin (DMY) has oxidation resistance, anti-inflammatory and free radical scavenging capabilities. The preventive effects of DMY for vascular hyporeactivity remain unclear.
OBJECTIVE
This study investigates the preventive effects of DMY in vascular hyporeactivity.
METHODS
The
Dihydromyricetin inhibits caerulin-induced TRAF3-p38 signaling activation and acute pancreatitis response.
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Acute pancreatitis (AP) is a common inflammatory disease in gastrointestinal tract. Our previous study has shown that caerulin induces TNF receptor-associated factor 3 (TRAF3)-p38 signaling activation and pro-inflammatory response in macrophages, causing damage to co-cultured pancreatic acinar
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