木樨草素拮抗庆大霉素耳毒性实验观察

目的:初步了解木樨草素对庆大霉素耳毒性的影响。方法:设庆大霉素组与庆大霉素加不同剂量木樨草素(10mg、20 mg)两组,并进行组间比较,观察听性脑干反应(ABR)阈值、眼震电图(ENG)的频率,了解其听功能及前庭功能的变化。结合耳蜗基底膜铺片琥珀酸脱氢酶(SDH)染色方法观察耳蜗形态学变化。结果:听功能检查结果显示,庆大霉素加不同剂量木樨草素组的ABR阈值明显低于庆大霉素组,经统计学处理,差异有显著性。形态学检查结果与听功能检查结果一致。前庭功能检查结果亦发现木樨草素对庆大霉素引起的前庭功能变化有拮抗作用。结论:本实验发现木樨草素对庆大霉素引起的耳蜗和前庭损伤有拮抗作用。     

木犀草素对实验性自身免疫性脑脊髓炎大鼠SPH/SPHK1/S1P1通路及神经元凋亡的影响

目的 探讨木犀草素(Luteolin)对实验性自身免疫性脑脊髓炎(Experimental autoimmune en-cephalomyelitis,EAE)大鼠神经酰胺-鞘氨醇(Sphingosine,SPH)/鞘氨醇激酶1(Sphingosine kinase 1,SPHK1)/1-磷酸鞘氨醇受体1(Sphing...     

高效液相色谱法测定甘肃金银花中槲皮素和木樨草素的含量

目的建立高效液相色谱(HPLC)法测定甘肃金银花中槲皮素和木樨草素含量的方法。方法采用Krom asil C18柱,以甲醇-水(60∶40)为流动相,磷酸调节pH值至3.5,流速:1.0 m l.m in-1,检测波长350 nm。结果槲皮素在2.93~35.16μg.m-l1;木樨草素在5.45~43.60μg.m-l1范围内呈良好线性关系,r槲=0.999 9,r木=0.999 7。平均回收率:槲皮素为96.2%,RSD=1.7%;木樨草素为96.5%,RSD=2.2%。结论甘肃金银花中槲皮素和木樨草素的含量远高于正品金银花。该方法灵敏度高,重现性好,可作为金银花质量评价的分析方法。     

紫背金盘草中木犀草素的定性分析

目的：确定紫背金盘草中是否含有木犀草素,为紫背金盘草中活性成分的确定和药理作用的研究提供参考。方法：采用薄层色谱法和高效液相法。条件,色谱柱为KromasilC18（4.6 mm×250 mm,5μm）,流动相为甲醇-0.2%磷酸溶液（56∶44,pH3）;流速0.8 ml/min;进样量20μl;紫外检测波长254 nm;柱温25℃。结果：通过薄层色谱法和高效液相法可得出紫背金盘草中不含木犀草素。结论：木犀草素可能不是紫背金盘具有抑菌、抗感染、消肿止痛的活性成分。     

HPLC法测定市售杭白菊中2种有机酸和2种黄酮的含量

摘 要 目的： 测定市售杭白菊中有效成分的含量,比较不同产地杭白菊质量。方法: 采用HPLC法测定绿原酸、3,5-O-双咖啡酰基奎宁酸2种有机酸成分以及木犀草苷、木犀草素2种黄酮成分的含量。结果: 收集杭白菊样品各有效成分差异较大,12批市售杭白菊绿原酸含量在0.22%～0.70%之间,木犀草苷含量在0.09%～0.25%之间,3,5-O-双咖啡酰基奎宁酸含量在0.84%～1.67%之间,木犀草素含量在0.008%～0.042%之间。结论: 市售杭白菊质量有较大差异,有必要进一步加强质量控制。     

高效液相色谱法测定北刘寄奴药材中木犀草素和毛蕊花糖苷的含量(英文)

建立了北刘寄奴药材中木犀草素和毛蕊花糖苷的反相高效液相含量测定方法。采用Agilent Zorbax SB-Aq C18 column (250 mm×4.6 mm, 5 μm) 色谱柱; 0.05%磷酸 (A) 和甲醇 (B) 梯度洗脱; 流速1.0 mL/min; 检测波长310 nm和350 nm。木犀草素和毛蕊花糖苷分别在0.0341-0.8172 mg/mL (r2 = 0.9999)和0.0708-2.832 mg/mL (r2 = 0.9999)范围内与峰面积呈良好的线性关系。平均加样回收率分别为102.7%和98.3%。15批北刘寄奴药材中木犀草素和毛蕊花糖苷的含量差异明显。本文首次报道了北刘寄奴药材中毛蕊花糖苷的含量测定方法。     

HPLC法测定益心巴迪然吉布亚颗粒中木犀草素的含量

目的:建立测定益心巴迪然吉布亚颗粒中木犀草素的高效液相色谱方法.方法:色谱柱:Shim-pack ODS(5μm,250 ×4.6mm);检测波长:350nm;流动相:甲醇-0.4％磷酸(48∶52);流速:1.00mL·min-1;柱温:35℃.结果:木犀草素在20μg·mL-1～120μg·mL-1间呈良好的线性关系,r =0.9998(n =5),日内精密度RSD为1.81％(n=5),日间精密度RSD为1.85％,稳定性RSD为1.55％(n=5),重复性RSD为0.36％(n=5),平均回收率为99.92％ (n =9),RSD为0.07％(n=9).结论:建立的定量方法操作简单、精密度高、重现性好,可以作为控制益心巴迪然吉布亚颗粒质量的有效方法.     

抗宫炎片质量标准研究

目的:建立抗宫炎片质量控制标准。方法:采用薄层色谱法对方中的广东紫珠、益母草、乌药进行定性鉴别;用反相高效液相色谱法测定处方中广东紫珠有效成分木犀草素的含量。结果:在薄层色谱中可检出广东紫珠、益母草、乌药;木犀草素在4.75μg/ml—19.00μg/ml范围内呈良好的线性关系(R2=0.9998),平均回收率为100.2%,RSD为0.67%。结论:所建立的方法能准确地进行定性、定量检测,可用于该制剂的质量控制。     

Luteolin promotes mitochondrial protection during acute and chronic periods of isoproterenol induced myocardial infarction in rats

ObjectiveAn attempt has been made to evaluate the mitochondrial protection in acute and chronic periods after isoproterenol (ISO)-induced myocardial-infarction (MI) in male Wistar rats.Materials and methodsLuteolin was supplemented by intra-gastric intubation at a daily dose of 0.3 mg/kg body weight for 30 days. In the acute MI model, luteolin had been administered once per day to rat groups during 30 days. On 29th and 30th days, the rats of the acute MI control groups were administered 85 mg/kg body weight, isoproterenol, intra-peritoneally at an interval of 24 h. In the chronic MI model luteolin was supplemented to the rat group during 30 days. On the 1st and 2nd days, the rats of the chronic MI control and luteolin treatment groups were administered ISO by the same way.ResultsThe isoproterenol-treated rats both in acute and chronic models showed an increase in the level of TBARS and a decrease in the activities of mitochondrial antioxidants in MI rats, an increase in levels of mitochondrial lipid profile except phospholipids and the activities of mitochondrial enzymes were decreased in isoproterenol-treated rats. Oral treatments with luteolin in both acute and chronic models showed a significant decrease in the levels of mitochondrial lipid peroxidation, increase in the mitochondrial antioxidant levels and also decrease in the mitochondrial enzymes.ConclusionThus the present study revealed that luteolin ameliorates mitochondrial damage in isoproterenol induced myocardial infarction by maintaining lipid peroxidation metabolism due to its free radical scavenging, mitochondrial lipids, antioxidants and mitochondrial enzymes. Histopathological observations were also in correlation with the biochemical parameters.     

Suppressive Effects of the Flavonoids Quercetin and Luteolin on the Accumulation of Lipid Rafts after Signal Transduction via Receptors

Quercetin (QUER) and luteolin (LUTE) are dietary flavonoids capable of regulating the production of cytokines, such as tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6). However, their mechanisms of action are not fully understood. In lipopolysaccharide-triggered (LPS)-triggered signaling via Toll-like receptor 4 (TLR4), QUER and LUTE suppresses not only the degradation of the inhibitor of κB (IκB), with resultant activation of nuclear factor-κB (NF-κB), but also the phosphorylation of p38 and Akt in bone marrow-derived macrophages that have been stimulated with LPS. We report here that, in TNF-α-induced signaling, QUER and LUTE significantly suppressed the production of IL-6 and activation of NF-κB. Accumulation of lipid rafts, the initial step in the signaling pathway, was significantly inhibited when macrophages were treated with QUER or with LUTE prior to exposure to LPS. Similarly, the accumulation of lipid rafts was inhibited by the flavonoids when B cells were activated via the membrane IgM and when T cells were activated via CD3. In contrast, QUER and LUTE did not inhibit the activation of phorbol myristate acetate-induced NF-κB in macrophages. Our observations suggest that QUER and LUTE interact with receptors on the cell surface and suppress the accumulation of lipid rafts that occurs downstream of the activation of the receptors.