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目的:建立HPLC法同时测定白芷中花椒毒酚、佛手柑内酯、欧前胡素和异欧前胡素含量的方法,比较不同产地白芷的成分含量变化。方法:采用Zorbax SB-C18色谱柱(150 mm×4.6 mm,5μm),流动相组成为乙腈和水,线性梯度洗脱,检测波长300 nm,流速1.0 ml·min-1。结果:在一定的浓度范围内,花椒毒酚、佛手柑内酯、欧前胡素和异欧前胡素的浓度与峰面积线性关系良好且具备良好的加样回收率。结论:本试验建立的HPLC方法简便易行,可用于白芷中4个活性成分的含量测定。 相似文献
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花椒毒酚的药效学研究:Ⅲ镇痛作用 总被引:8,自引:0,他引:8
花椒毒酚是从蛇床子中提取的一种呋喃香豆素。XT明显抑制醋酸引起的小鼠扭体反应。XT显著提高热板法致痛小鼠的痛阈,此作用不被阿片受体拮抗剂纳络酮所拮抗。此外,XT明显降低大鼠角叉菜胶足跖炎痛组织内PGE含量。这些结果表明XT确有镇痛作用,其镇痛机制主抑制PG的合成而非激动阿片受体。 相似文献
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花椒毒酚(xanthotoxol,XT)是从蛇床子中提取出的一种呋喃香豆素。XT对二甲苯所致小鼠耳壳肿胀、醋酸引起的小鼠腹腔毛细血管通透性增高、大鼠角叉菜胶性足跖肿胀均有明显的抑制作用,对小鼠棉球肉牙肿增生也有明显的抑制作用。结果表明XT对急性和慢性炎症模型均有抗炎作用。此外,XT明显降低大鼠角叉菜胶性足跖炎症组织内PGE含量。 相似文献
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摘 要 目的:建立HPLC梯度洗脱法同时测定康妇软膏中异土木香内酯、土木香内酯、花椒毒酚、氧化前胡素、欧前胡素和蛇床子素的含量。 方法: 以Agilent TC C18(250 mm×4.6 mm,5 μm)为色谱柱,甲醇 0.1%甲酸溶液为流动相,梯度洗脱,流速0.9 ml·min-1 ,检测波长分别为220 nm和300 nm,柱温35 ℃。 结果:异土木香内酯、土木香内酯、花椒毒酚、氧化前胡素、欧前胡素和蛇床子素分别在6.16~123.20 μg·m-1 、3.78~75.60 μg·m-1 、1.87~37.40 μg·m-1 、4.06~81.20 μg·m-1 、9.27~185.40 μg·m-1 、13.89~277.80 μg·m-1 范围内线性关系良好,相关系数分别为0.999 4,0.999 8,0.999 6,0.999 5,0.999 9和0.999 7;平均加样回收率分别为98.04%(RSD=1.06%),97.10%(RSD=1.53%),96.73%(RSD=0.90%),98.92%(RSD=1.36%),99.12%(RSD=0.83%)和100.27%(RSD=0.58%)。结论:该方法简便、准确,可用于康妇软膏质量标准的提高。 相似文献
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《Neuro-Chirurgie》2023,69(3):101426
BackgroundOxidative damage and inflammation are two critical mechanisms underlying secondary brain injury (SBI) following intracerebral hemorrhage (ICH). Xanthotoxol is reported to alleviate brain edema and inhibit inflammatory responses. Herein, we investigated the effects of xanthotoxol and its related mechanisms in SBI post-ICH.MethodsTo explore the clinical effects of xanthotoxol an animal model of ICH was established. Neurological scores, survival rates and brain water content were measured. Inflammatory responses and oxidative damage in the peri-hemorrhagic areas were determined by measuring pro-inflammatory cytokines and oxidative related factors. The activation of the M1/M2 phenotype was detected by western blotting and immunofluorescence.ResultsXanthotoxol improved the neurological functions and reduced cerebral edema in ICH mice. Additionally, xanthotoxol inhibited microglia activation and promotes microglial phagocytosis. Simultaneously, xanthotoxol promoted the transformation of BV2 cells from M1 phenotype to M2 phenotype, and protected BV2 cells against hemin-induced inflammation and oxidative stress. Mechanistically, xanthotoxol inactivated the NF-κB p65 signaling pathway in the hemin-challenged BV2 cells.ConclusionXanthotoxol ameliorates SBI post-ICH by suppressing microglia-mediated neuroinflammation and oxidative stress and enhancing microglial phagocytosis through inhibition of NF-κB signaling. 相似文献
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