isoginkgetin/inflammation

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Anti-inflammatory effects of chemical components from Ginkgo biloba L. male flowers on lipopolysaccharide-stimulated RAW264.7 macrophages.

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Ginkgo biloba L., well known as living fossil, have various pharmacological activities. Eighteen compounds were isolated from Ginkgo male flowers including a novel matsutake alcohol glycoside, Ginkgoside A (1), and 17 known compounds-calaliukiuenoside (2), benzylalcohol O-α-l-arabinopyranosyl-(1 →

Effects of Ginkgetin from Ginkgo biloba Leaves on cyclooxygenases and in vivo skin inflammation.

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Ginkgetin, a biflavone from Ginkgo biloba leaves, was previously reported to be a phospholipase A2 inhibitor and this compound showed the potent antiarthritic activity in rat adjuvant-induced arthritis as well as analgesic activity. This investigation was carried out to find effects on

Biflavonoids from Caper (Capparis spinosa L.) fruits and their effects in inhibiting NF-kappa B activation.

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Caper (Capparis spinosa L.) fruits have been widely used as food and folk medicine in the Mediterranean basin and in central and west Asia. In this study, two biflavonoids, isoginkgetin, and ginkgetin, together with three other flavonoids, were isolated from caper fruits. Their chemical structures

Effects of flavonoids of Ginkgo biloba on proliferation of human skin fibroblast.

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Ginkgo biloba studies have focused on the anti-inflammatory effects of the major components, ginkgolide and bilobalide, whereas little is known about their effect on fibroblasts. This study demonstrated the enhancing effects of Ginkgo L. extracts, especially the flavonoid fractions: quercetin,

Inhibition of arachidonate release from rat peritoneal macrophage by biflavonoids.

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Biflavonoid is one of unique classes of naturally-occurring bioflavonoid. Previously, certain biflavonoids were found to possess the inhibitory effects on phospholipase A(2) activity and lymphocytes proliferation(1) suggesting their anti-inflammatory/immunoregulatory potential. In this study,

Alternatively spliced isoforms of IL-32 differentially influence cell death pathways in cancer cell lines.

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Alternative splicing is a biological mechanism that enables the synthesis of several isoforms with different or even opposite functions. This process must be tightly regulated to prevent unwanted isoform expression favoring pathological processes. Some isoforms of interleukin 32 (IL-32) are reported

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