Bioactivity of Traditional Chinese Herbal Medicines Against Pyricularia oryzae

Two hundred and four species of traditional Chinese herbal medicines belonging to 80 families were collected from Yunnan Province in People’s Republic of China and tested for antifungal activities using a Pyricularia oryzae bioassay. Twenty-six herbal medicines from 23 families were active against P. oryzae and the ethanol extract of Dioscorea camposita (Dioscoreaceae) exhibited the most bioactivity among all the tested samples.     

丙泊酚静脉麻醉对急性重型颅脑损伤手术患者的脑保护作用探讨

目的 探讨丙泊酚静脉麻醉对急性重型颅脑损伤手术患者的脑保护作用.方法 选择急性重型颅脑损伤手术患者70例,按入院顺序随机分成对照组与观察组,每组35例.观察组静脉给予丙泊酚2 mg/kg进行麻醉诱导,然后以4 mg·kg-1·h-1维持;对照组给予咪达唑仑0.06 mg/kg进行麻醉诱导,然后间断吸入异氟烷维持.两组患者静脉麻醉诱导均加用丙泊酚1.2 mg/kg,芬太尼4μg/kg,维库溴铵0.15 mg/kg.记录麻醉前、术中和术后3h患者颅内压和脑氧分压的变化情况,且记录患者术后初醒时间.结果 两组术后3h与麻醉前比较颅内压明显下降,脑氧分压明显升高;且观察组的颅内压明显低于对照组[(18.98±3.98) mm Hg与 (21.76±4.01) mm Hg](t=7.20,P＜0.05),脑氧分压明显高于对照组[(17.09±3.03) mm Hg与(14.67 ±2.63)mm Hg](t=7.23,P＜0.05),观察组的初醒时间短于对照组[(15.98±2.01)h与(20.01±1.23)h](t=7.96,P＜0.05).结论 丙泊酚静脉麻醉对急性重型颅脑损伤手术患者具有良好的脑保护作用,值得临床推广应用.     

JAK-STAT pathway modulates the roles of iNOS and COX-2 in the cytoprotection of early phase of hydrogen peroxide preconditioning against apoptosis induced by oxidative stress

Our previous studies have demonstrated that preconditioning with hydrogen peroxide (H₂O₂) activated the JAK-STAT pathway that played an important role in the cytoprotection, and inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mediated the late phase of cytoprotection induced by high concentration of H₂O₂ after preconditioning. Here we sought to identify the downstream targets of the JAK-STAT axis that mediated H₂O₂ preconditioning and the expression of iNOS and COX-2 in the early phase of H₂O₂ preconditioning. It was shown that (1) Preconditioning with H₂O₂ at 100 μmol/L for 90 min in PC12 cells induced significant expression of iNOS and COX-2. (2) Pretreatment with the iNOS inhibitor AG (10 μmol/L) or the COX-2 inhibitor NS-398 (10 μmol/L) respectively 20 min before H₂O₂ preconditioning not only inhibits the increased expression of iNOS or COX-2 but also abrogates the protective effects of H₂O₂ preconditioning against apoptosis induced by oxidative stress. (3) Pretreatment with the JAK inhibitor AG-490 (10 μmol/L) 20 min before H₂O₂ preconditioning obviously inhibits the up-regulation of iNOS or COX-2 induced by H₂O₂ preconditioning. These results suggested that JAK-STAT pathway modulates the roles of iNOS and COX-2 in the cytoprotection of early phase of H₂O₂ preconditioning.     

氨磷汀在血液肿瘤治疗中的应用与展望

 虽然干细胞移植治疗血液肿瘤取得了良好疗效,但大剂量放疗及化疗治疗血液肿瘤仍很重要,放疗或化疗对正常组织造成的严重损伤限制了其要达到的治疗效果。达到最大的治疗效果并对正常细胞和组织产生最小的破坏作用是临床工作者追求的目标。氨磷汀（商品名：阿米福汀）是无机硫代磷酸盐细胞保护剂,它的化学名是S-2-[（3-氨基丙基）氨基]-硫代乙醇磷酸酯。它是一种前体药物,活性成分为游离的硫羟基,可以清除细胞毒性药物在组织中产生的自由基。它是一种广谱选择性细胞保护剂,能保护多种正常组织免受化疗及放疗的损伤。造血干细胞移植前预处理中使用氨磷汀可以减轻血液学、肾脏毒性,在化疗中使用氨磷汀可以减轻化疗药物如顺铂、环磷酰胺和长春碱等造成的肾脏毒性。文章就氨磷汀的药理特性及在血液肿瘤治疗中的细胞保护作用进行综述。     

亚砷酸联合阿米福汀对HL-60细胞中Survivin表达的影响

 目的　探讨亚砷酸（As2O3）联合阿米福汀（AMI）诱导人髓系白血病细胞HL-60凋亡的可能机制。方法　不同浓度As2O3单用和联合AMI对HL-60细胞进行不同时间干预,用MTT比色法检测细胞的生长抑制作用,用半定量RT-PCR法检测抑凋亡基因Survivin mRNA的表达水平。结果　As2O3组和联合组均可显著抑制HL-60细胞的增生,呈浓度依赖性,联合组对其抑制作用明显大于As2O3组。联合组降低Survivin的表达作用比As2O3组更明显。结论　As2O3通过下调抑凋亡基因Survivin的表达诱导HL-60凋亡;AMI可增强As2O3对Survivin的下调作用,增强HL-60细胞对As2O3的敏感性,发挥促凋亡效应。     

党参等中药对胃粘膜的快速保护作用

目的 为观察党参、大黄、丹参、疏肝调胃汤等中药对胃粘膜的快速保护作用及中药胃粘膜快速保护作用的普遍性。方法 采用先给大鼠胃饲药物,随后立即胃饲2ml无水乙醇的方法,分别观察党参、大黄、丹参煎剂及疏肝调胃汤对大鼠胃粘膜损伤的影响。结果 （1）预先胃饲党参煎剂10g/kg显著抑制大鼠胃粘膜损伤,损伤抑制率为79．9％;（2）预先胃锔大黄煎剂12g/kg,损伤抑制率为48．1％;（3）预先胃饲丹参煎剂12g/kg,损伤抑制率为61．35％;（4）预先胃饲疏肝调胃汤6g/kg,损伤抑制率为56．84％;预先胃饲疏肝调胃汤12g/kg,损作抑制率为79．79％。结论 党参、大黄、丹参和疏肝调胃汤均对胃粘膜有快速保护作用,在单味中药中党参作用最短,丹参次之,大黄最弱。     

前列腺素对阿斯匹林诱发大鼠急性胃粘膜损伤的保护作用

本文从不同形态学水平观察前列腺素（Ｐｒｏｓｓｔａｇｌａｎｄｉｎ Ｅ２，ＰＧＥ２）对阿斯匹林诱发大鼠急性胃粘膜损伤的保护作用，结果表明：预先给予ＰＧ，能完全抑制胃粘膜大体病变，明显减轻粘膜深层的组织损伤，部分保护粘膜上皮细胞脱落。的描电镜下，可见胃腺体粘液分泌旺盛，腺颈细胞向胃小凹表面移行。显示ＰＧ对胃粘膜产生形态学上的保护作用，其机理与促进粘液分泌、加速上皮修复有关。     

Verapamil and flunarizine protect the isolated perfused rat liver against warm ischemia and reperfusion injury

Using the model of the isolated perfused rat liver, we investigated the influence of the two pharmacologically different calcium channel blockers, verapamil and flunarizine, on changes of ion homeostasis, liver weights, pH deviations and enzyme activities during warm ischemia (37°C) and reperfusion. The LDH and GLDH activities were determined and the calcium, potassium, and sodium concentrations were measured in the effluent. Warm ischemia (180 min) caused an increased enzyme release, a high influx of calcium and sodium into the liver and a massive potassium efflux current. Normoxic reperfusion led to a further increase in hepatic enzyme release and although the loss of potassium ceased, the calcium influx into the liver continued. By the end of reperfusion the liver weight had increased significantly (P<0.01) in the control group. The two calcium entry blockers were added to the perfusate in various concentrations. Both substances protected the liver against warm ischemia and normoxic reperfusion damage, but they did not inhibit calcium inflow. However, the potassium efflux was significantly reduced by all concentration tasted (P<0.001). After reperfusion the liver weights were significantly lower in the treated groups (P<0.001) than in control animals. Thus, the calcium entry blockers verapamil and flunarizine protect liver cells against damage caused by warm ischemia and reperfusion. Furthermore, they prevent the disruption of intracellular potassium homeostasis, which seems to be related to improved volume regulation of liver cells.     

CYTOPROTECTION OF THE DIGESTIVE TRACT

Cytoprotection is rather a new concept with a history of about 15 years. It wasoriginated from the finding that prostaglandins (PGs) had a cytoprotective effect on thegastric mucosa. We then proposed the hypothesis that cytoprotection might be one of thephysiological functions of gut peptides. There have been increasing evidences in theliterature to support our hypothesis. Here we present the findings from our laboratoryon the cytoprotection of gastric mucosa, pancreas and liver. We believe strongly thatcytoprotection is an important concept with theoretical and practical implications.     

氨磷汀在体外减轻足叶乙甙所致的骨髓间充质干细胞损伤

目的研究氨磷汀在体外对化疗药物所致的骨髓间充质干细胞（MSCs）损伤的影响，为其应用于慢性粒细胞白血病（CML）患者的造血干细胞移植提供实验依据。方法采集CML患者的骨髓细胞，应用极限稀释法获取单克隆来源的MSCs，并在低血清培养液中培养和扩增。按实验分组分别加入氨磷汀（氨磷汀组）、足叶乙甙（VP-16组）、氨磷汀和足叶乙甙（联合处理组），并设没有处理的对照组。在药物作用一定时间后，计数MSCs，绘制生长曲线；流式细胞仪检测MSCs的免疫表型及凋亡率；在甲基纤维素半固体培养中检测MSCs作为滋养层支持造血的能力。结果MSCs生长曲线显示，与对照组相比，氨磷汀组的MSCs生长未受明显影响，联合处理组MSCs的生长显著好于沿16组。培养48h后，对照组、氨磷汀组、联合处理组和VP-16组的MSCs凋亡率分别为（4．9±0．8）％、（5．6±1．2）％、（18．7±3．4）％和（33．8±5．1）％，氨磷汀组与对照组相比，差异无统计学意义；联合处理组高于对照组，但明显低于VP-16组（P〈0．05）。形成粒-单核系集落、红系集落和多系集落的产率，氨磷汀组与对照组间的差异无统计学意义，联合处理组低于对照组（P〈0．05），但显著高于VP-16组（P〈0．05）。氨磷汀作用前后未见MSCs免疫表型发生明显改变。结论氨磷汀在体外对CML患者骨髓来源MSCs的增殖、凋亡、造血支持能力以及免疫表型无明显影响，但能显著改善足叶乙甙对MSCs所致的生长抑制及功能损伤，提示在预处理中加用氨磷汀可能成为促进CML患者造血干细胞移植后造血恢复的一种新策略。