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中藥標準品

山奈酚

文字:[大][中][小] 2017-4-27    瀏覽次數(shù):1890    


產(chǎn)品編號
英文名稱
CAS號
包裝
 Y3653
 Kaempferol  
520-18-3
可根據(jù)客戶要求訂制
產(chǎn)品編號:Y3653

英文名稱:Kaempferol  
CAS號:520-18-3
分析標準品,≥98%  
分子式 C15H10O6 分子量286.24  


基本信息:


密度  1.688
熔點   276°C
存貯條件   儲存溫度 -20°C
描述  
別名   山奈酚 ;莰菲醇,3,4',5,7-四羥基黃酮;3,4',5,7-Tetrahydroxyflavone 3,5,7-Trihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one Robigenin
生化機理  
Description: IC50 value: Kaempferol inhibits proliferation of ovarian cancer cells at 40μM or higher concentrations[2]. Kaempferol (3,5,7-trihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one) is a relatively common nontoxic, natural dietary compound which has been reported to reduce the risk of ovarian cancer[1]. in vitro: Kaempferol was found to inhibit estrogen receptor alpha expression in breast cancer cells and to induce apoptosis in glioblastoma cells and lung cancer cells by activation of MEK-MAPK. Studies have shown that kaempferol also has anti-inflammatory effects via inhibition of interleukin-4 and cyclo-oxygenase 2 expression by suppressing Src kinase and downregulating the NFκB pathway. Kaempferol is also effective in inhibiting angiogenesis and inducing apoptosis in ovarian cancer cells [1]. kaempferol has a distinct epigenetic activity by inhibition of histone deacetylases (HDACs). In silico docking analysis revealed that it fits into the binding pocket of HDAC2, 4, 7 or 8 and thereby binds to the zinc ion of the catalytic center. Further in vitro profiling of all conserved human HDACs of class I, II and IV showed that kaempferol inhibited all tested HDACs [4]. in vivo: Male BALB/c mice with ALI, induced by intranasal instillation of LPS, were treated or not with Kae (100 mg/kg, intragastrically) 1h prior to LPS exposure. Kae treatment attenuated pulmonary edema of mice with ALI after LPS challenge, as it markedly decreased the lung W/D ratio of lung samples, protein concentration and the amounts of inflammatory cells in BALF[3]. Clinical trial:N/A  
應用   一種黃酮醇。能使佛波醇酯處理的小鼠成纖維細胞或v-H-ras-轉(zhuǎn)化的 NIH 3T3細胞變形后的恢復。能顯著誘導核DNA退化,同時伴隨脂類的過氧化反應。抑制拓撲異構(gòu)酶I催化的DNA再連接。



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