固脱汤对失血性休克大鼠血浆NO、6—keto—PGF1α和TXB2含量的影响

目的和方法：观察固脱汤对失血性休克大鼠血浆NO、6－keto-PGF1α和TXA2含量的影响。结果：失血性休克大鼠血浆NO水平增高（P＜0．01），6－keto－PGF1α含量明显降低（P＜0．01），TXA2含量增高（P＜0．01），固脱汤加可明显升高血浆NO、6－keto-PGF1α水平（P＜0．01），而血浆TXB2含量未见显著性改变（P＞0．05）。结论：固脱汤可通过促进血管内皮细胞产生和释放NO及PGI1发挥抗休克作用。     

糖尿病大鼠阴茎海绵体内PGI2，TXA2含量变化的研究

目的：探讨前列环素（PGI2）与血栓塞A2（TXA12）在糖尿病性阳萎发病过程中的作用,方法：以四氧嘧啶诱导的四月龄雄性Wistar大鼠为糖尿病模型,模型成功后3周,以放射免疫分析方法检测糖尿病组及对照组大鼠阴茎海绵体内PGI2和TXA2含量。结果：糖尿病大鼠阴茎海绵体内PCI2含量较对照组明显下降（P＜0．01）,TXA2含量增高（P＜0．05）,结论：PGI2与TXA2比较失衡是糖尿病性阳萎的病因之一。     

吲哚美辛对梗阻性黄疸血清β2—MG的影响

目的 观察吲哚美辛（Ind)对梗阻性黄疸（梗黄）血清β2－MG水平的影响。方法 用放射免疫分析法检测18例服用Ind的梗黄患。服药前后及术后第4天血清及尿液中β2－微球蛋白（β2－MG）的水平，并同期检测其血浆血栓素（TXA2）、前列环素（PGI2）的含量。结果 服用Ind后随着TXA2／PGI2的下降，血清β2－MG亦明显下降（P＜0．05），但不能恢复至正常水平，且尿β2－MG无变动。结论 Ind可通过抑制TXA2的生成，在一定程度内降低梗黄病人血清β2－MG的水平。     

水蛭醇提物与水提物对肺缺血再灌注模型大鼠的保护作用

目的：研究水蛭醇提物与水提物对肺缺血再灌注模型大鼠的保护作用,并比较两者的作用效果。方法：夹闭阻断大鼠左肺门30min,开放后再灌注120min以复制肺缺血再灌注损伤模型。32只SD大鼠随机分为假手术（等容生理盐水）组、模型（等容生理盐水）组、水蛭醇提物（400mg／kg）组、水蛭水提物（400mg／kg）组。于术前3d腹腔注射给药,每天1次,连续3d。放射免疫法测定大鼠血浆血栓素B2（TXB2）和6酮前列腺素F1a（6-keto-PGF1a）含量[可反映血栓素A2（TXA2）、前列环素（PGI2）水平];酶联免疫吸附法测定大鼠血清一氧化氮（NO）含量与一氧化氮合酶（NOS）活性。结果：与假手术组比较,模型组大鼠血浆中TXB2含量显著增加,TXB2／6．keto-PGF1a比值显著降低,血清中NO含量显著增加,NOs活性显著增强（P〈0．01或P〈0．05）;与模型组比较,水蛭醇提物组、水蛭水提物组大鼠血浆TXB2、6-keto-PGF1a含量显著减少,TXB2／6．keto—PGF1a比值显著升高,血清N0含量显著减少,NOS活性显著减弱（P〈0．01或P〈0．05）,且以上指标水蛭醇提物组均好于水蛭水提物组,但差异无统计学意义（P〉0．05）。结论：水蛭醇提物与水蛭水提物均可降低肺缺血再灌注模型大鼠TXA2、PGI2、NO含量和NOS活性,且前者效果好于后者。     

蒙药“珍珠-25”味对动脉粥样硬化大鼠血脂代谢的影响

目的：观察蒙药“珍珠-25”味对动脉粥样硬化（AS）大鼠血清的血脂代谢的影响,探讨蒙药“珍珠-25”味抗AS的作用机制。方法：基于文献,采用腹腔注射维生素D3及喂养高脂饲料方法复制动脉粥样硬化大鼠模型,模型建立后,随机将大鼠分为4组。即空白组、模型组、血脂康治疗组、蒙药治疗组,各组进行相应干预,通过观察及检测各组大鼠血清TC、TG、LDL—C和HDL—C等变化,分析蒙药“珍珠-25”味对AS的治疗作用。结果：与空白组比较,模型组大鼠血清TC、TG、LDL—C增高（P〈0．01）,血清HDL—C明显降低（P〈0．01）;而与模型组比较,蒙药“珍珠-25”味能明显升高模型大鼠血清HDL—C（P〈0．01）,降低大鼠血清TC、TG、LDL—C（P〈0．01）,且与阳性对照组比较,差异无统计学意义。结论：蒙药“珍珠-25”味能调节动脉粥样硬化大鼠脂质代谢异常,对AS大鼠模型有治疗作用。     

新化合物哌芳安他抗大鼠和兔动脉粥样硬化作用机理的初步研究

目的在早期和晚期动脉粥样硬化模型上研究新化合物哌芳安他抗动脉粥样硬化的机制.方法大鼠或家兔随机分为正常对照、模型对照和哌芳安他给药组,其中模型对照和哌芳安他给药组动物给予高胆固醇饲料,检测的指标包括:兔颈动脉HE染色;大鼠或兔血清TC, LDL-CHO, HDL-CHO, IL-8, ET-1, PGI2, TXA2 和NO水平;兔颈动脉MCP-1和 IL-8 mRNA表达量.结果哌芳安他能明显抑制早期和晚期动脉粥样硬化中TXA2的过量表达,在大鼠早期动脉粥样硬化中可见哌芳安他给药组动物血清NO增加而IL-8含量减少;在兔晚期动脉粥样硬化中可见IL-8和MCP-1 mRNA表达降低;哌芳安他对血脂水平、MDA 和SOD无明显影响.结论哌芳安他抗动脉粥样硬化机制与其升高血清NO水平,降低TXA2含量及抑制IL-8 和MCP-1过度表达相关.     

六味地黄方对高脂血症大鼠血浆 ET、TXA2、PGI2水平及动脉内皮保护的影响

目的：研究六味地黄方对高脂血症大鼠血浆ET、TXA2、PGI2水平及动脉血管内皮保护的影响。方法：通过高脂饮食建立高脂血症大鼠模型,观察大鼠外周循环内皮细胞（CEC）、主动脉病理学、内皮素（ET）、前列腺素I2（PGI2）、血栓素A2（TXA2）的变化。结果：六味地黄方能减少高脂血症大鼠外周CEC及主动脉内皮细胞损伤;降低高脂大鼠血清ET、血浆TXA2,升高血浆PGI2水平。结论：六味地黄方对高脂血症大鼠内皮细胞具有保护作用,其作用机制可能与改善内皮细胞分泌功能有关。     

心复宁V号对垂体后叶素致急性心肌缺血大鼠血浆TXA2及PG12的影响

目的:观察心复宁V号对垂体后叶素所致急性心肌缺血大鼠血浆TXA2及PGI2的影响。方法:60只大鼠,随机分成6组,即空白对照组、模型对照组、心复宁V号大剂量组(17.08g/kg)、心复宁V号中剂量组(8.54 g/kg)、心复宁V号小剂量组(4.27g/kg)、阳性对照组(单硝酸异山梨酯)。采用灌胃给药,每天1次,连续14d。末次给药后1h,舌下静脉给予垂体后叶素造成急性心肌缺血模型。1h后取血,分离血浆,测定各组TXA2、PGI2的代谢产物6-Keto-PGF1a、TXB2,分析PGI2/TXA2比值。结果:大鼠给予垂体后叶素后,血浆中TXB2升高,6-Keto-PGF1a/TXB2比值降低(P<0.05、0.01)。与模型对照组比较,心复宁V号(17.08g/kg,8.54 g/kg)明显降低垂体后叶素所升高的TXB2,升高6-Keto-PGF1a/TXB2(P<0.01)。结论:心复宁V号抗垂体后叶素致大鼠心肌缺血作用机制之一是通过抑制升高的血浆TXA2,纠正PGI2/TXA2失衡。     

二参颗粒对心肌缺血大鼠血清TXA2/PGI2的平衡及炎症细胞因子水平的影响

摘要：目的:通过检测二参颗粒对心肌缺血大鼠血清学相关指标的影响,探讨二参颗粒抗心肌缺血的机制。方法:将50只健康Wistar大鼠按随机数字表法分为5组:正常对照组、模型组、二参颗粒高、中、低剂量组(35.2,17.6,8.8 g·kg-1),每组10只。连续灌胃给药2周后,除正常对照组外,其余4组大鼠用垂体后叶素(20 U·kg-1)腹腔注射建立心肌缺血模型后记录心电图标Ⅱ导联变化,TUNEL染色观察大鼠心肌细胞凋亡情况,检测血清血栓素A2（TXA2）、前列环素（PGI2）的含量及炎症细胞因子白细胞介素1（IL-1）、白细胞介素6（IL-6）和白细胞介素10（IL-10）的水平。结果:与正常对照组相比,模型组各时间点ST段J点变化值及T波变化值、心肌细胞凋亡指数、血清TXA2含量、IL-1及IL-6水平明显增加,PGI2含量、IL-10水平明显降低（P<0.05）。与模型组相比,二参颗粒部分剂量组各时间点ST段J点变化值及T波变化值显著降低,3个剂量组心肌细胞凋亡指数、血清TXA2含量、IL-1及IL-6水平显著降低,PGI2含量、IL-10水平显著增加（P<0.05）。结论:二参颗粒能调节TXA2/PGI2的平衡,改善血清炎症细胞因子水平,从而抑制血管内皮炎症性改变,保护血管内皮功能,达到抗心肌缺血作用。     

川芎嗪对妊娠高血压综合征患者血浆TXA2／PGI2平衡的调节和肾功能的影响

目的探讨川芎嗪对妊娠高血压综合征患者血浆TXA2／PGI2平衡的调节和肾功能的影响。方法选择40例轻中度PIH患者．予以川芎嗪120mg静滴10d（川芎嗪治疗组）,另取正常妊娠对照组30例。采用放射免疫法测定血浆TXA2和PGI2的稳定代谢产物TXB2和6-keto-PGF1a浓度。而正常妊娠对照组只测定1次。结果川芎嗪治疗组治疗前与正常妊娠对照组相比较,血浆TXA2含量上升,血浆PGI2含量下降（均P〈0．05）。经过川芎嗪治疗10天后,患者血浆TXA2含量下降。血浆PGI2含量上升（均P〈0．05）;川芎嗪治疗组治疗前与正常妊娠对照组相比较。尿U-MALB和β2-MG均显著升高（P〈0．01）．经过川芎嗪治疗10天后,尿U—MALB和β2-MG明显降低（P〈0．05）。结论川芎嗪具有降低PIH患者血浆TXA2含量和升高PGI2含量,纠正TXA2／PGI2失衡作用,同时川芎嗪还具有提高PIH患者肾小球滤过率和增加肾小管重吸收功能。降低尿蛋白排泄量。保护肾功能作用。     

Molecular mechanisms of the protective role of wheat germ oil against cyclosporin A-induced hepatotoxicity in rats

Abstract

Context: Cyclosporin A (CsA) is one of the most important immunosuppressive agents. However, its clinical use is strongly limited by several side effects including hepatotoxicity which remains a major clinical problem. Involvement of reactive oxygen species (ROS) in CsA-induced hepatotoxicity has been reported.

Objective: This study investigates the potential protective role of wheat germ oil (WGO) as an antioxidant against CsA-induced hepatotoxicity.

Materials and methods: Twenty-four male Wistar albino rats (six animals in each group) received castor oil, the vehicle of CsA i.p. (control) or either CsA (25?mg/kg/d i.p.), WGO (900?mg/kg/d by oral gavage), or CsA in combination with WGO daily for 21?d.

Results: CsA administration significantly increased serum levels of the liver enzymes alanine aminotransferase (ALT) and aspartate aminotransferase (AST). In addition, an increase in lipid peroxidation, inducible NO-synthase (iNOS), and NF-κB expression were observed in hepatic tissues of CsA-alone-treated rats. Furthermore, significant reduction in the hepatic content of reduced glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) was also observed in CsA-alone-treated animals. Moreover, histopathological changes occurred in CsA-alone-treated rats. Concomitant administration of WGO along with CsA improved all these parameters. Most interestingly, the immunosuppressive effect of CsA was not affected by WGO.

Conclusion: The present study suggests that concomitant use of WGO might be useful in reducing liver toxicity induced by CsA via inhibition of ROS, iNOS, and NF-κB expression.     

新化合物PPVP在大鼠动脉粥样硬化模型上抗动脉粥样硬化分子机制的研究

目的　研究新化合物PPVP抗动脉粥样硬化作用的分子机制。方法　在高血脂诱发大鼠早期动脉粥样硬化模型上 ,观察PPVP给药组动物血液及血管组织中重要的动脉粥样硬化相关因子表达的情况。结果　PPVP对血脂 ,ET 1和PGI2 水平无明显影响 ,但明显增加血清中NO含量 ,降低血清TXA2 含量 ,抑制趋化因子IL 8的过度表达。结论　PPVP的上述作用特点可能与其抗动脉粥样硬化作用相关     

低分子肝素对肾病综合征大鼠血栓素A_2及前列环素表达的影响

目的探讨低分子肝素(LMWH)对肾病综合征(NS)大鼠肾脏保护作用的可能机制。方法将雄性SD大鼠随机分为正常对照组、肾病综合征模型组、肾病综合征模型加低分子肝素治疗组,分别于2、3、4周留取24 h尿,测定尿蛋白,并离心沉淀备测血栓素A2(TXA2)和前列环素(PGI2),同时腹主动脉取血测定血清白蛋白。结果肾病综合征大鼠尿中TXA2明显增加,随病变发展逐渐升高。而PGI2没有明显变化。LMWH治疗后尿中PGI2浓度升高,24 h尿蛋白减少,血清白蛋白升高。结论LMWH可增加NS大鼠尿中PGI2浓度,纠正TXA2/PGI2比值失衡,是其保护肾脏的可能机制之一。     

Relationship between eicosanoids and endothelin-1 in the pathogenesis of erythropoietin-induced hypertension in uremic rats

Recent studies suggest a possible link between recombinant human erythropoietin (rhEPO)-induced hypertension and endothelium-derived vasoconstrictor autocoids. The current study was designed to evaluate the role of eicosanoids such as thromboxane (TX) A and prostacyclin (PGI ) and of endothelin-1 (ET-1) and the relationship between these vasoactive substances in rhEPO-induced hypertension in uremic rats. Renal failure was induced by a two-stage 5/6 nephrectomy followed by a 6-week stabilization period. In protocol A, rats were divided into four groups: vehicle, rhEPO (100 u/kg, subcutaneously, three times per week), a selective ET receptor antagonist (ABT-627, 10 mg/kg/d), and rhEPO + ABT-627 for 5 weeks. In protocol B, uremic animals were divided into two groups: rhEPO and rhEPO + a TX receptor antagonist and synthesis inhibitor, ridogrel (25 mg/kg/d), for 5 weeks. At the end of the study, immunoreactive eicosanoid metabolites (TXB and 6-keto-PGF, stable metabolites of TXA and PGI ), and ET-1 were measured in either the thoracic aorta or in the mesenteric arterial bed. After 5/6 nephrectomy, the animals developed uremia, anemia, and hypertension. rhEPO corrected the anemia but aggravated the hypertension. Both drugs were effective in preventing the progression of hypertension in rhEPO-treated rats although ABT-627 was more potent than ridogrel. rhEPO increased the concentration of ET-1 and TXB in blood vessels and ABT-627 decreased tissue levels of both vasopressors. The concentration of 6-keto-PGF was not significantly changed. Ridogrel significantly decreased tissue TXB concentrations but had no effect on ET-1 levels. These results suggest that endothelium-derived vasoconstrictor autacoids (TXA and ET-1) are involved in the pathogenesis of rhEPO-induced hypertension in uremic rats. TXA probably serves as a mediator of the vascular effect of ET-1.     

Effect of etersalate on human platelet responsiveness. A study in healthy volunteers

Ex vivo antiplatelet properties of 2-(p-acetamido-phenoxy)ethyl-o-acetoxybenzoate (etersalate, Daital) and its effects on serum thromboxane A2 (TXA2) levels and prostaglandin I2 (PGI2) generation were studied in human volunteers at two levels of oral dosing. Etersalate inhibited at the lower dosage platelet function and decreased TXA2 levels, but PGI2 generation from rat aortic rings was stimulated when incubated with plasma from etersalate-treated donors. Blood coagulation parameters remained within normal values. It is suggested that etersalate administration could act on platelet arachidonate metabolism at a different level than that of the cyclooxygenase pathway.     

Alterations in prostacyclin and thromboxane formation by chronic cigarette smoke exposure: temporal relationships and whole smoke vs. gas phase

Chronic cigarette smoke exposure in vivo causes decreased conversion of [14C]arachidonic acid (AA) to prostacyclin (PGI2) by isolated aortic tissue and increased conversion to thromboxane (TXA2) by isolated platelets from rats. Alterations in the PGI2/TXA2 balance may be part of the mechanism through which smoking increases the risk of cardiovascular disease. To study the influence of smoke exposure duration on this response, male rats were exposed daily to 10 puffs of freshly generated cigarette smoke. Animals were killed after 1, 4, 14, 28 and 57 days of smoke exposure and 3, 7, 14 and 28 days after cessation of the 57-day of smoke-exposure regimen. Elevated carboxyhemoglobin levels during the smoke-exposure sessions verified smoke (gas phase) inhalation. Statistically significant alterations in prostacyclin synthesis preceded those of thromboxane. A decrease of 20-25% (P less than 0.05) in PGI2 production from [14C]AA in isolated aortic tissue was found beginning 28 days after smoke was initiated and quickly rebounded when smoke exposure was terminated. Increased production of TXA2 from [14C]AA by isolated platelets became statistically significant (P less than 0.05) on the 57th day and returned to normal 7-14 days after cessation of smoke exposure. To determine the effect of gas phase constituents on the PGI2/TXA2 balance a second series of experiments divided male and female Sprague-Dawley rats into sham, whole smoke and gas phase groups. Gas phase was produced by passing whole smoke through a Cambridge filter to remove particulate matter. Per cent COHb averaged 1.4 for sham, 7.8 for whole smoke and 9.4 for gas phase groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

复方丹参滴丸对动脉粥样硬化患者血管内皮细胞分泌功能的影响

目的研究复方丹参滴丸对血管内皮细胞分泌功能的保护作用,探讨其机制。方法选择动脉粥样硬化患者200例,入选患者实验前采空腹静脉血检测ET、PGI2、TXA2,然后给与复方丹参滴丸10丸/次,3次/d,服用3个月,再采空腹静脉血检测ET、PGI2、TXA2,自身前后对照研究。结果患者实验前的ET、TXA2明显较高,而PGI2水较低,而给与复方丹参滴丸干预后再检测ET、PGI2、TXA2,服药前相反,ET、TXA2明显降低（P〈0.01）,而PGI2明显升高（P〈0.01）。结论复方丹参滴丸能够调整、改善血管内皮细胞分泌功能的异常状态,血管内皮细胞可能是复方丹参滴丸作用的靶点之一。     

An investigation of the ability of elemene to pass through the blood‐brain barrier and its effect on brain carcinomas

Objectives Elemene is a chemical extracted from plants. It has demonstrated anti‐tumour capability. Although widely studied, there has been little reported regarding its tissue distribution. Our aim was to rectify this. Methods The tissue distribution of elemene was studied after intragastric or intravenous administration in rats. The effectiveness of elemene in treating brain tumours was studied using the G‐422 tumour cell model in mice. Key findings Elemene had a higher concentration in the lungs, spleen and livers than other tissues of normal rats after intragastric and intravenous administration, while the concentration in the gastrointestinal tract was greater after intragastric administration. Elemene molecules were also detected in the rats' brain tissue. Elemene had a therapeutic effect on mice inoculated with G‐422 cells both intracranially and subcutaneously. The best life‐extending rate and the best tumour‐inhibiting rate of elemene were 64.43% and 34.46%, respectively, when 80 mg/kg elemene was used for treatment. Conclusions The results from the tissue distribution study showed that elemene can pass through the blood‐brain barrier. The therapeutic experiments showed that elemene is effective in treating cerebral malignancy.