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991.
T Takahashi H Takami S Sadahiro Y Okuda S Kodaira 《Gan to kagaku ryoho. Cancer & chemotherapy》1985,12(5):1158-1159
992.
The effects of various flavonoids [i.e. baicalein, baicalin, wogonin, skullcapflavone II, (2 S),2',5,6',7-tetrahydroxyflavanone, (2 R,3 R),2',3,5,6',7-pentahydroxyflavanone, and 2',5,5',7-tetrahydroxy-6',8-dimethoxyflavone] isolated from Scutellariae Radix on rat peritoneal polymorphonuclear leukocyte lipoxygenase and cyclooxygenase products were studied. Baicalein (5,6,7-trihydroxyflavone) was found to inhibit the formation of 5-HETE (lipoxygenase product) more strongly than the formation of HHT (cyclooxygenase product); its concentrations for 50% inhibition (IC (50)) were 7.13 +/- 0.767 microM for the formation of 5-HETE and 55.3 +/- 16.9 microM for the formation of HHT (cyclooxygenase product). Baicalin (baicalein-7- O- D-glucuronide) also inhibited the formation of 5-HETE, though less strongly, while its compound had no effect on the formation of HHT (cyclooxygenase product) in polymorphonuclear leukocytes. In contrast, (2 S),2',5,6',7-tetrahydroxyflavanone inhibited the formation of HHT more strongly than the formation of 5-HETE via 5-lipoxygenase pathway; its concentrations for IC (50) were 5.63 +/- 1.27 microM for the formation of HHT and 670.0 + 85.0 microM for the formation of 5-HETE. Wogonin and (2 R,3 R),2',3,5,6',7-pentahydroxyflavanone also inhibited the formation of HHT; their IC (50) values were respectively 14.6 +/- 3.51 microM and 50.0 +/- 4.04 microM. 相似文献
993.
Glucocorticoids are well known for their anti-inflammatory effect through the regulation of gene expression in many types of immune cells, including mast cells. However, the genes that are involved in suppression of mast cell-mediated inflammation by glucocorticoids have not been fully identified. Therefore, we examined the dexamethasone (Dex)-responsive genes in RBL-2H3 mast cells using a high-density oligonucleotide microarray technique. Gene expression profiling revealed that the antigen-induced up-regulation of pro-inflammatory factors, including monocyte chemoattractant protein-1, was markedly inhibited by 100 nM Dex. On the other hand, Dex treatment itself caused the substantial up-regulation of many genes, including phenylethanolamine-N-methyl transferase (PNMT) and cytokine-inducible SH2-containing protein (CISH), in the mast cells. The expression of these two genes significantly increased 6 h after Dex exposure and lasted for more than 24 h. Considering that PNMT is the rate-determining enzyme in epinephrine synthesis and that CISH is a suppressor of cytokine signaling, these Dex-responsive genes may be potential anti-inflammatory factors. Thus, gene expression profiling suggested that Dex might exert its anti-inflammatory effect through two pathways in mast cells: the suppression and induction of potentially pro- and anti-inflammatory factors, respectively. 相似文献
994.
Ulifloxacin is the active form of the prodrug prulifloxacin and shows a highly potent antipseudomonal activity. In this study, we examined the combined effect of fosfomycin and ulifloxacin against Pseudomonas aeruginosa (P. aeruginosa) growing in a biofilm using a modified Robbins device with artificial urine, and compared it to that of the combination of fosfomycin and ciprofloxacin or levofloxacin. An ATP bioluminescence assay was used to evaluate the antibacterial activity of the agents against sessile cells in a mature biofilm developed on a silicon disk. The total bioactivity of P. aeruginosa growing in a biofilm that had not been fully eradicated by fosfomycin or any of the fluoroquinolones alone at 10 times the MIC decreased after combination treatment with fosfomycin and fluoroquinolones. Morphological changes occurred in a time-dependent fashion; namely, swollen and/or rounding cells emerged within a couple of hours after combination treatment, marking the initial stage in the process leading to the destruction of the biofilms. We could not find any difference among the 3 fluoroquinolones with regard to their synergistic effects when administered with fosfomycin. The combination treatment of fosfomycin and fluoroquinolones with highly potent antipseudomonal activities was effective in eradicating sessile cells of P. aeruginosa in the biofilm and promises to be beneficial against biofilm-associated infectious diseases. 相似文献
995.
996.
Takao T Kumagai C Hisakawa N Matsumoto R Hashimoto K 《The Journal of endocrinology》2005,184(1):191-197
We determined the effect of 17beta-estradiol on tumor necrosis factor alpha (TNF-alpha)-induced cytotoxicity in human peripheral T lymphocytes (T cells) using lactate dehydrogenase assay. Treatment with 17beta-estradiol (1-100 nM) for 24 h showed dose-dependent reduction of TNF-alpha-induced cytotoxicity in T cells. To further evaluate the mechanism of 17beta-estradiol on TNF-alpha-induced cytotoxicity in T cells, we identified estrogen receptor (ER) protein in T cells using immunocytochemistry and used the pure ER antagonist ICI 172,780. ERalpha immunoreactivity was clearly observed in T cells. ERbeta immunoreactivity was also detected in some T cells. ICI 172,780 (10(-7) M) alone did not affect cytotoxicity in T cells, however, ICI 172,780 (10(-7) M) completely abolished 17beta-estradiol cytoprotective effects in T cells. TNF-alpha tended to increase nuclear factor kappaB (NF-kappaB) protein levels in nuclear extracts but it did not reach statistical significance by Western blotting. In contrast, NF-kappaB protein levels in nuclear extracts followed by TNF-alpha with 17beta-estradiol treatment were significantly increased compared with NF-kappaB protein levels in untreated group. NF-kappaB blocker pyrrolidinedithiocarbamate (PDTC) (10(-4) M) alone did not affect cytotoxicity in T cells. In contrast, PDTC (10(-4) M) completely abolished 17beta-estradiol cytoprotective effects in T cells. Caspase -3/-7 activity was significantly increased followed by TNF-alpha, and 17beta-estradiol treatment significantly reduced the increment. The present studies suggest the protective effect of 17beta-estradiol on TNF-alpha-induced cytotoxicity through ERs in T cells and that NF-kappaB activation and caspase suppression may be involved in the mechanism. 相似文献
997.
PURPOSE: Glaucomatous visual field loss and optic disc damage differ by intraocular pressure (IOP) levels. In this study, we compared the optic disc topography in the high-tension group and the low-tension group in normal-tension glaucoma (NTG). METHOD: We selected NTG patients with mean deviation (MD) > or = -10.00 dB and the highest recorded IOP of < 14 mmHg or > or = 17 mmHg without glaucoma treatment. We classified NTG eyes into the following two groups: 1) a low-tension group with the highest recorded IOP of < 14 mmHg, 2) a high-tension group with the highest recorded IOP of > or = 17 mmHg. The optic disc parameters in the low-tension group eyes were compared with those in the high-tension group eyes using a Heidelberg Retina Tomograph. RESULTS: Nineteen eyes of nineteen patients were selected for each group. The cup/disc area ratio in the global sector, and the rim volume in the nasal sector of the low-tension group had deteriorated more than in the high-tension group. CONCLUSIONS: The disc topography is different between the low-tension group and the high-tension group in the nasal sector, suggesting that different pathogenetic mechanisms exist in the optic disc damage in NTG. 相似文献
998.
999.
Kanai Y Tatsumi Y Tokiwa T Watanabe Y Fujimaki T Ishiyama D Okuda T 《The Journal of antibiotics》2005,58(8):507-513
Two new antifungal antibiotics, F2928-1 (1) and -2 (2), were isolated from the culture broth of Cladobotryum sp. These compounds were purified by solvent extraction, silica gel column chromatography and preparative HPLC, consecutively. The structures of these compounds were assigned as a decalin compound on the basis of various spectral analyses. These compounds showed antimicrobial activity against fungi including clinically important fungus, Aspergillus fumigatus. 相似文献
1000.