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bakkenolide/reazioni di ipersensibilità
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6 risultati
Anti-allergic and anti-inflammatory effects of bakkenolide B isolated from Petasites japonicus leaves.
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OBJECTIVE
To elucidate the anti-allergic and anti-inflammatory effects of Petasites genus, we studied the effects of several compounds isolated from Petasites japonicas leaves.
METHODS
Bakkenolide B was isolated from Petasites japonicus leaves. Antigen-induced degranulation was measured in RBL-2H3
Anti-allergic effects of total bakkenolides from Petasites tricholobus in ovalbumin-sensitized rats.
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The anti-allergic effect of total bakkenolides from the rhizome of Petasites tricholobus (BAPT) was evaluated in an ovalbumin-induced allergic rhinitis model in male Wistar rats. The major components of the bakkenolide fraction are bakkenolide-D, bakkenolide-B, bakkenolide-IIIa and bakkenolide-IVa,
Bakkenolides and Caffeoylquinic Acids from the Aerial Portion of Petasites japonicus and Their Bacterial Neuraminidase Inhibition Ability
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Petasites japonicus have been used since a long time in folk medicine to treat diseases including plague, pestilential fever, allergy, and inflammation in East Asia and European countries. Bioactive compounds that may prevent and treat infectious diseases are identified based on their ability
Petatewalide B, a novel compound from Petasites japonicus with anti-allergic activity.
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BACKGROUND
The giant butterbur Petasites japonicus is used to treat asthma and allergic diseases in traditional Korean, Japanese, and Chinese medicine.
OBJECTIVE
To elucidate the anti-allergic effect of Petasites genus, we studied effects of several compounds from Petasites japonicus leaves and
Bakkenolide G, a natural PAF-receptor antagonist.
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Because platelet-activating factor (PAF, 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine) participates in many physiopathological responses, including inflammatory reaction, endotoxic shock, allergic diseases and platelet aggregation, PAF-receptor antagonists are important in the treatment of these
Petasites japonicus bakkenolide B inhibits lipopolysaccharide‑induced pro‑inflammatory cytokines via AMPK/Nrf2 induction in microglia.
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Abnormal neuroinflammatory responses have diverse roles in neuronal death, oxidative stress and neurodegenerative diseases, such as Alzheimer's and Parkinson's disease. Microglia regulate these responses via molecular signaling cascades that involve inflammatory cytokines and complement proteins.
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