Papyriflavonol A from Broussonetia papyrifera inhibits the passive cutaneous anaphylaxis reaction and has a secretory phospholipase A2-inhibitory activity.
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Papyriflavonol A, a new prenylated flavonol isolated from Broussonetia papyrifera, selectively inhibits recombinant human secretory phospholipase A(2)s (sPLA(2)s). Papyriflavonol A was found to inhibit human group IIA and V sPLA(2)s potently and irreversibly in a dose-dependent manner, with respective IC(50) values of 3.9 and 4.5 microM. The inhibitory effects of papyriflavonol A against bovine group IB (IC(50) of 76.9 microM) and the human group X (IC(50) of 225 microM) sPLA(2)s were weaker than those against human group IIA and V sPLA(2)s, and human group IIF sPLA(2) was not inhibited. In addition, papyriflavonol A potently inhibited the stimulus-induced production of leukotriene C(4) with an IC(50) value of approximately 0.64 microM in mouse bone marrow-derived mast cells. In addition, papyriflavonol A significantly reduced IgE-dependent passive cutaneous anaphylaxis in rats. These results indicate that papyriflavonol A provides a basis for novel types of antiinflammatory drugs. (+info)
Comparison with various parts of Broussonetia papyrifera as to the antinociceptive and anti-inflammatory activities in rodents.
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This study compared the antinociceptive and anti-inflammatory effects of various parts of Broussonetia papyrifera (L.) L'Herit. ex Vent. (BP, Moraceae) by chemical-induced pain and inflammation in rodents. All BP parts (1 and 2 g/kg, p.o.) effectively inhibited writhing responses induced by 1% acetic acid. The BP radix, leaf, and fruit effectively inhibited the late-phase licking responses caused by 1% formalin. But only the BP radix and fruit reduced the edema induced by 1% carrageenan at 1-2 h. Furthermore, the BP radix reduced the abdominal Evan's blue extravasations caused by inflammatory mediators, including serotonin and sodium nitroprusside. Finally, the radix had the highest contents of betulin and betulinic acid among all BP parts. In conclusion, the radix is the better medicinal BP part possessing antinociceptive and antiinflammatory effects, and its anti-inflammatory effects are partially related to the inhibition of vascular permeability via autocrines and nitric oxide. (+info)
Inhibitory effects of heartwood extracts of Broussonetia kazinoki Sieb on the development of atopic dermatitis in NC/Nga mice.
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We investigated the effects of a topically applied extract of the heartwood of Broussonetia kazinoki Sieb (B. kazinoki) on atopic dermatitis (AD)-like skin lesions induced by an extract of the house-dust mite Dermatophagoides farina in NC/Nga mice. We found that topically applied B. kazinoki extract suppressed the histological manifestations of AD-like skin lesions, and decreased the levels of plasma immunoglobulin E (IgE) and interleukin-4 (IL-4) in the mice. Moreover, B. kazinoki inhibited the induction of thymus-and-activation-regulated chemokine (TARC/CCL17), macrophage-derived chemokine (MDC/CCL22), and regulated-on-activation-normal T cell-expressed-and-secreted chemokine (RANTES/CCL5) in HaCaT cells activated by tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma). In conclusion, our results suggest that B. kazinoki extract has therapeutic advantages in the treatment of AD. (+info)
Fungicidal effect of prenylated flavonol, papyriflavonol A, isolated from Broussonetia papyrifera (L.) vent. against Candida albicans.
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Papyriflavonol A (PapA), a prenylated flavonoid (5,7,3',4'-tetrahydroxy-6,5'-di-(r,r-dimethylallyl)-flavonol), was isolated from the root barks of Broussonetia papyriferra. Our previous study showed that PapA has a broad-spectrum antimicrobial activity against pathogenic bacteria and fungi. In this study, the mode of action of PapA against Candida albicans was investigated to evaluate PapA as antifungal agent. The minimal inhibitory concentration (MIC) values were 10~25 microgram/ml for C. albicans and Saccharomyces cerevisiae, gram-negative bacteria (Escherichia coli and Salmonella typhimurium) and gram-positive bacteria (Staphylococcus epidermidis and Staphylococcus aureus). The kinetics of cell growth inhibition, scanning electron microscopy, and measurement of plasma membrane florescence anisotrophy revealed that the antifungal activity of PapA against C. albicans and S. cerevisiae is mediated by its ability to disrupt the cell membrane integrity. Compared with amphotericin B, a cell membrane disrupting polyene antibiotic, the hemolytic toxicity of PapA was negligible. At 10~25 microgram/ml of MIC levels for the tested strains, the hemolysis ratio of human erythrocytes was less than 5%. Our results suggest that PapA could be a therapeutic fungicidal agent having a broad spectrum antimicrobial agent. (+info)
Kazinol Q from Broussonetia kazinoki enhances cell death induced by Cu(II) through increased reactive oxygen species.
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A prenylated flavan from Broussonetia kazinoki prevents cytokine-induced beta-cell death through suppression of nuclear factor-kappaB activity.
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The generation of nitric oxide (NO) via inducible NO synthase (iNOS) and reactive oxygen species plays a key role in cytokine-mediated pancreatic beta-cell damage. Oxidative stress due to reactive oxygen species activates the nuclear factor-kappaB (NF-kappaB) transcription factor, which regulates iNOS expression. In this regard, suppression of the NF-kappaB pathway is a novel strategy for protecting beta-cells from damage. This study was performed to explore the effects of kazinol U, a prenylated flavan from Broussonetia kazinoki, on the NF-kappaB activation pathway in interleukin-1beta (IL-1beta)- and interferon-gamma (IFN-gamma)-treated beta-cells. The cytotoxic effects of cytokines were completely abolished when RINm5F cells or islets were pretreated with kazinol U. Kazinol U inhibited the nuclear translocation and DNA binding of NF-kappaB subunits, which correlated with the inhibitory effects on IkappaB kinase (IKK) phosphorylation and IkappaBalpha degradation. In addition, kazinol U suppressed NO and hydrogen peroxide production and apoptotic cell death by cytokines in RINm5F cells. The protective effects of kazinol U were further demonstrated by normal insulin secretion of cytokine-treated islets in response to glucose. Taken together, these results suggest that using kazinol U to block the NF-kappaB pathway in pancreatic beta-cells reduces cell damage. Therefore, kazinol U may have therapeutic value in delaying pancreatic beta-cell destruction in type 1 diabetes. (+info)
Chemical composition and antioxidant activities of Broussonetia papyrifera fruits.
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