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不同医疗机构紫草饮片质量评价
胡国冰;雒琪;赵雪梅
中国医院药学杂志 2011年 31卷16期 页码:1344-1347页,共4页 影响因子:0.663
紫草;高效液相色谱法;左旋紫草素;β,β′-二甲基丙烯酰阿卡宁;含量测定
目的:调查不同医疗机构的紫草饮片的质量.方法:参照中国药典2010年版的方法,用薄层色谱法对购自不同医疗机构的紫草进行鉴别,采用紫外分光光度法、高效液相色谱法对上述紫草饮片进行含量测定.结果:通过对紫草饮片样品与对照品的薄层色谱比较,确定紫草饮片的薄层色谱中含有与对照品相同斑点,用紫外分光光度法测定出左旋紫草素成分含量均符合中国药典规定,但含量差异很大;β,β′-二甲基丙烯酰阿卡宁的线性方程为y= 23 372X+ 77 437,r=0.999 7,β,β′-二甲基丙烯酰阿卡宁在7.5~500.0μg·mL-1范围内线性关系良好,平均回收率为98.39%,RSD为1.09%.用高效液相色谱法测定出7个紫草样品中有6个β,β ′-二甲基丙烯酰阿卡宁成分含量高于中国药典2010年版规定的最低限量.结论:紫草饮片含量差异很大.
益气养阴方对小鼠肝癌及子宫颈癌肺转移抑制作用的实验研究
弭玮;孙静
大连医科大学学报 2009年 31卷4期 页码:247-250页,共4页 影响因子:0.633
益气养阴方;血道转移;淋巴道转移;自发性转移
[目的]观察益气养阴方对小鼠肝癌及子宫颈癌肺转移的抑制作用.[方法]H22肝癌细胞悬液经小鼠尾静脉接种,观察荷瘤小鼠的肺部转移瘤情况;小鼠右下肢爪垫内侧皮下注射接种,复制淋巴道转移模型,观察小鼠实体瘤的瘤重量、抑瘤率、肺部转移率、淋巴结转移情况.U14子宫颈癌细胞悬液经小鼠肌肉接种,复制自发性转移模型,观察小鼠实体瘤的瘤重量、抑瘤率、肺部转移率.[结果]血道转移模型结果:中药组肺瘤结节数较造模组下降(21.13±7.95 v 34.11±12.14,P<0.05).淋巴道转移模型结果表明:中药组肺瘤结节数、淋巴结指数较造模组均有下降(4.5±2.619 v 8.3±3.917和0.702±0.182 v 0.89±0.181,P<0.05).自发转移模型结果:中药组移植瘤生长指数、肺转移瘤生长指数较造模组比均明显降低(0.059±0.013 v 0.086±0.024,P<0.01,3.899±1.356 v 5.035±1.336,P<0.05).[结论]益气养阴方对小鼠移植性肿瘤的生长及转移均有明显抑制作用,且能明显抑制肺转移瘤的生长.
注射用普鲁卡因细菌内毒素检查法可行性研究
雒琪;王复馨;李军
天津药学 2003年 15卷1期 页码:4-6页,共3页 影响因子:0.715
动态浊度法;凝胶法;细菌内毒素;普鲁卡因
目的:建立普鲁卡因注射液的细菌内毒素检查方法(动态浊度法,凝胶法),以控制药品质量,减少临床热原反应的发生.方法:按<中国药典>2000版附录中细菌内毒素检测法及细菌内毒素检测法指导原则的规定[1],系统考察注射用普鲁卡因对鲎试剂与细菌内毒素凝集反应的干扰,确定用于细菌内毒素动态浊度法和凝胶法的不干扰浓度.结果:将注射用普鲁卡因配制成1%浓度经20倍稀释后可应用动态浊度法定量检测;凝胶法最佳检测条件为:供试品1∶20稀释,鲎试剂灵敏度(λ)=0.25 EU/ml.结论:应用动态浊度法定量检测普鲁卡因注射液细菌内毒素含量,结果准确;凝胶法可用于日常检测.细菌内毒素检查法可替代家兔法用于普鲁卡因注射液的热原检查.
Cardioprotection of Ginkgolide B on Myocardial Ischemia/Reperfusion-Induced Inflammatory Injury via Regulation of A20-NF-kappa B Pathway
Zhang, R;Xu, L;Zhang, D;Hu, B;Luo, Q;Han, D;Li, JB;Shen, CW
FRONTIERS IN IMMUNOLOGY 2018年 9卷
NF-KAPPA-B; REPERFUSION INJURY; TNF-ALPHA; INHIBITION; ACTIVATION; PROMOTES; A20; INFARCTION; ISCHEMIA; PROTECTS
Inflammation urges most of the characteristics of plaques involved in the pathogenesis of myocardial ischemia/reperfusion injury (MI/RI). In addition, inflammatory signaling pathways not only mediate the properties of plaques that precipitate ischemia/reperfusion (I/R) but also influence the clinical consequences of the post-infarction remodeling and heart failure. Here, we studied whether Ginkgolide B (GB), an effective anti-inflammatory monomer, improved MI/RI via suppression of inflammation. Left anterior descending (LAD) coronary artery induced ischemia/reperfusion (I/R) of rats or A20 silencing mice, as well as hypoxia/reoxygenation (H/R) induced damages of primary cultured rat neonatal ventricular myocytes or A20 silencing ventricular myocytes, respectively, served as MI/RI model in vivo and in vitro to discuss the anti-I/R injury properties of GB. We found that GB significantly alleviated the symptoms of MI/RI evidently by reducing infarct size, preventing ultrastructural changes of myocardium, depressing Polymorphonuclears (PMNs) infiltration, lessening histopathological damage and suppressing the excessive inflammation. Further study demonstrated that GB remarkably inhibited NF-kappa B p65 subunit translocation, I kappa B-alpha phosphorylation, IKK-beta activity, as well as the downstream inflammatory cytokines and proteins expressions via zinc finger protein A20. In conclusion, GB could alleviate MI/RI-induced inflammatory response through A20-NF-kappa B signal pathway, which may give us new insights into the preventive strategies for MI/RI disease.
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