当归醇沉物对体外小鼠脾、胸腺淋巴细胞增殖的影响

体外试验中,采用ＭＴＴ比色法测定当归醇沉物对小鼠脾及胸腺淋巴细胞增殖功能的影响,结果显示,０．１６～２．５０ｍｇ／ｍＬ范围内的当归醇沉物能单独或协同ＣｏｎＡ／ＬＰＳ发挥促进小鼠脾脏及胸腺Ｔ,Ｂ淋巴细胞增殖的作用,当归醇沉物尚可对氢化泼尼松（ＨＰ）对ＣｏｎＡ诱导的脾脏及胸腺Ｔ淋巴细胞的增殖反应的抑制作用。     

腹腔注射硝酸甘油小鼠心、脑、肾一氧化氮含量的变化

介绍了腹腔注射硝酸甘油后小鼠心、脑、肾一氧化氮含量随时间、剂量变化的关系。结果可见 ,5min内心、脑组织中一氧化氮含量迅速上升 ,10min之后开始下降 ,2 0min后基本恢复正常。肾中一氧化氮含量在 2 0min达到最大值 ,6 0min后基本恢复正常。在 6 .0mg/kg硝酸甘油的剂量范围内 ,心、脑、肾组织中一氧化氮含量呈剂量依赖关系     

大蒜素对乙醇引起肝损伤的拮抗作用

研究大蒜的有效成分大蒜素对乙醇氧化性肝损伤的影响。结果表明大蒜素（１０ｍｇ／ｋｇｉｇ，ｑｄ×１０）不仅能逆转乙醇所致血清丙氨酸转氨酶和谷胱甘肽Ｓ－转移酶活性的升高，而且能明显增加乙醇肝损伤小鼠肝脏谷胱甘肽含量、谷胱甘肽过氧化物酶、谷胱甘肽还原酶和谷胱甘肽Ｓ－转移酶活性。对乙醇所致肝脏丙二醛含量、超氧化物歧化酶和过氧化氢酶活性的改变则无明显影响。提示大蒜素能拮抗乙醇氧化性肝损伤，其机制与增强肝脏谷胱甘肽抗氧化系统的功能有关     

血清谷胱甘肽S-转移酶在小鼠急性硫代乙酰胺肝损伤中的诊断价值

探讨了血清谷胱甘肽Ｓ－转移酶（ＧＳＴ）对硫代乙酰胺（ＴＡＡ）所致小鼠急性肝损伤的早期诊断意义。结果表明，腹腔注射ＴＡＡ２５～１００ｍｇ／ｋｇ能增加小鼠血清ＧＳＴ活性，其活性改变与ＴＡＡ之间存在量－效和时－效关系，与血清ＡＬＴ变化间呈高度正相关。ＴＡＡ致血清ＧＳＴ活性明显异常的同时，肝谷胱甘肽含量和ＧＳＴ、谷胱甘肽过氧化物酶和超氧化物歧化酶活性明显降低。提示肝脏抗氧化功能减退是ＴＡＡ致肝损伤的主要机理之一，血清ＧＳＴ水平是反映ＴＡＡ急性肝损伤的早期灵敏指标。     

复方缬芎滴丸对大鼠急性脑缺血的保护作用

目的 :研究复方缬芎滴丸对大鼠局灶性脑缺血的保护作用。方法 :采用线栓法造成大鼠一侧大脑中动脉永久性阻塞模型。通过大鼠行为学评分、脑梗塞指数、脑重指数及脑组织病理学改变等指标 ,观察复方缬芎滴丸抗急性脑缺血的作用。结果 :复方缬芎滴丸小剂量组 (31.3mg·kg-1)、中剂量组 (93.7mg·kg-1)、大剂量组 (15 6 .7mg·kg-1)均使脑缺血大鼠神经症状明显减轻 (P <0 .0 1) ,脑梗塞指数分别为 16 .5 2 %± 5 .78%、16 .5 4 %± 3.0 0 %、14 .18%± 6 .13% ,与阴性对照组脑梗塞指数 (2 4 .0 3%± 4 .85 % )相比 ,差异均有显著性 (P <0 .0 1)。HE染色显示各用药组神经元和组织间隙水肿程度明显减轻 ,波及范围明显缩小。结论 :复方缬芎滴丸有明显的抗急性脑缺血作用。     

羟基磷灰石和二氧化钛纳米粒子溶胶的血液相容性

羟基磷灰石 (HAP)和二氧化钛 (TiO2 )纳米粒子是两种具有潜在应用前景的生物材料。本文通过溶血实验、小鼠出血和凝血时间、凝血酶原时间 (PT)和白陶土部分凝血活酶时间 (PTT)测定等对两种纳米粒子溶胶的血液相容性行了初步评价。结果显示 ,HAP纳米粒子溶胶、溶血实验阴性 ,显著延长小鼠的出血、凝血时间和大鼠白陶土部分凝血活酶时间和凝血酶原时间。TiO2 纳米粒子溶胶对小鼠的出、凝血时间无影响 ,溶血实验阴性。对大鼠白陶土部分凝血活酶时间和凝血酶原时间也无影响。两种纳米粒子溶胶均可使体外家兔红细胞发生凝聚。上述实验不同的结果主要与使用了不同的稳定剂有关 :HAP稳定剂为肝素 ,TiO2 稳定剂为聚氯乙烯 (PVC)。提示 ,在考虑纳米粒子溶胶的生物学应用前景时 ,除了纳米粒子本身的性质 ,筛选具备生物学惰性的稳定剂也是不容忽视的问题     

小白鼠骨髓细胞的制备方法及其应用

采用简便、有效、实用、稳定的动物骨髓细胞制备方法研究放射线对骨髓细胞的影响以及药物的防治作用具有重要的实际意义，本文以小白鼠为实验对象，建立了一种小白鼠骨髓细胞的制备方法．该方法经济、简便、实用、易行，已被用于我们的科研实践中．     

Does CYP2E1 play a major role in the aggravation of isoniazid toxicity by rifampicin in human hepatocytes?

Isoniazid and rifampicin are first-line anti-tubercular drugs. In a recent paper, Shen et al. provided interesting findings that rifampicin exacerbated isoniazid toxicity in human hepatocytes but not in rat hepatocytes. The main conclusion was that the difference in cytochrome P450 2E1 (CYP2E1) induction by rifampicin between rat and human hepatocytes accounted for the difference in exacerbation of isoniazid hepatotoxicity by rifampicin. 4-Nitrophenol hydroxylase (4-NP) activity was the only probe of CYP2E1 activity used in the paper. The authors presented data showing that rifampicin enhanced 4-NP activity and CYP2E1 mRNA expression in human hepatocytes, but not in rat hepatocytes. However, CYP3A also makes a significant contribution to 4-NP activity in humans and rats, which has been confirmed by both CYP3A-specific inducer and inhibitors. Rifampicin is a strong inducer of human CYP3A; thus, the increase in 4-NP activity in human hepatocytes could be due to the induction of CYP3A. Rifampicin did not increase 4-NP activities in rat hepatocytes, which could reflect a lack of the induction of rat CYP3A by rifampicin. Additionally, more experiments are needed to support the conclusion that rifampicin increased CYP2E1 mRNA expression in human hepatocytes because of the small sample size and the limitations of semi-quantitative RT-PCR. The study by Shen et al. suggests that another drug-metabolizing enzyme rather than CYP2E1 could be involved in the aggravation of isoniazid toxicity by rifampicin in human hepatocytes.The 2008 paper by Shen et al. is available from http://www3.interscience.wiley.com/cgi-bin/fulltext/121667602/PDFSTART     

Disordered APC/C‐mediated cell cycle progression and IGF1/PI3K/AKT signalling are the potential basis of Sertoli cell‐only syndrome

The cause of Sertoli cell‐only syndrome (SCOS), a condition in which only Sertoli cells line the seminiferous tubules in the testis, is unknown. Three microarray data sets were downloaded from public databases and were used to compare SCOS and control group. A total of 291 genes differentially expressed (Log₂|FC| ≥ 1 and adjusted p value < 0.05) in SCOS patients. Further 238 genes were significantly downregulated, and 53 genes were significantly upregulated. To identify the hub genes in the differentially expressed genes, we constructed a protein–protein interaction network, and CCNB1, CCNA2, AURKA, KIF11, CCNB2, CDC6, PRC1, NCAPG, KIF2C and PLK4 were screened from the network for the downregulated genes. Since the upregulated genes could not form a network, we concentrated on the genes with a higher fold change, and CPA3, NFIB, LONRF2, LYVE1, ATP8B4, IGF1, ITPR1 and PLAT were identified as the top 50% fold change genes in any of the three microarray data sets. Among downregulated hub genes, CDC6, CCNA2, CCNB1 and CCNB2 were involved in APC/C‐mediated cell cycle progression. Among key upregulated genes, IGF1 was involved in the PI3K/AKT pathway, while the other genes have not been reported in Sertoli or Leydig cells. In conclusion, SCOS appears to be caused by disordered APC/C‐mediated cell cycle progression and PI3K/AKT signalling.     

P-450特异性化学抑制剂在外源化合物代谢中的作用

已知细胞色素Ｐ４５０（ｃｙｔｏｃｈｒｏｍｅＰ４５０,ＣＹＰ）单加氧酶系统在机体对外源化合物代谢中占有主导地位。随着研究水平的提高和手段的增加,人们对ＣＹＰ同工酶在外源化合物代谢中作用的认识日趋深入。近年来的大量研究已证实,人ＣＹＰ酶蛋白很难纯化,但化学抑制剂在确定参与外源化合物代谢的ＣＹＰ类型上却是非常有效的工具药［１～４］,化学抑制剂为预测药物间的相互作用,提供了有效的研究手段。１　人ＣＹＰ同工酶与外源化合物代谢ＣＹＰ是一组含亚铁血红素蛋白的超家族（ｓｕｐｅｒｆａｍｉｌｙ）,主要位于肝微粒…