The pharmacodynamics experiment of Xinkang injection protect action of ADR-induced toxin myocarditisin mice

Objective The experiment is to study the protective effects of Xinkang Injection on ADR-induced toxin myocarditisin mice.Methods The test of Xinkang Injection on ADR-induced toxin myocarditisin mice.Firstly,the animal of obnormal,weight and death rate.Secondly,the influnences of cardiogram of ADR-induced toxin myocarditisin mice.Thirdly,the influnences of lactate dehydrogenase(LDH),creatine kinase(CK)and glutamic oxaloacetic transaminasw(GOT)of ADR-induced toxin myocarditisin mice.Fouthly,the influnences of changes of cardioc pathological mechanism of ADR-induced toxin myocarditisin mice.Fifthly,the influnces of the caidioc ultrastructural of ADR-induced toxin myocarditisin mice.Results Firstly,to ADR-induced toxin myocarditisin mice,the weight of middle dose and high dose of Xinkang injection had declined obviosly which contrast with the constraction model mice team.In the mean time,the weight of Xinkang injection team had obviosly changde which contrast with contrastion mice team(P<0.01).Secondly,to ADR-induced toxin myocarditisin mice,the middle dose and high dose of Xinkang injection have obviosly withstand Q abnormal cardiogram,in the meantime,Xinkang injection team had obviosly changde contrast with the contrastion model mice(P<0.01).Thirdly,to ADR-induced toxin myocarditisin mice,The activity of lactate dehydrogenase(LDH),creatine kinase(CK)and glutamic oxaloacetic transaminasw(GOT)were differently measured.The middle dose and high dose of Xinkang injection team can obviously declined the activity of LDH and CK(P<0.01).Fouthly,to ADR-induced toxin myocarditisin mice,the low dose,the middle dose and high dose of Xinkang injection team can contrast with injured on toxic myocarditisin mice cardioc.Fifthly,to ADR-induced toxin myocarditisin mice,the low dose,the middle dose and high dose of Xinkang injection team have effect of allevite the injection of the cardioc ulteasteuctural of ADR-induced toxin myocarditisin mice.Conclusions Xinkang injection can protect the ADR-induced toxin myocarditisin mice.     

大蒜多糖对阿霉素所致小鼠心脏毒性的拮抗作用

目的　研究大蒜多糖 (GP)对中毒性心肌炎的拮抗作用并探讨其机制。方法　建立小鼠阿霉素 (ADR)中毒性心肌炎模型,测定血清、心肌多项生化指标,并观察心肌结构变化。结果　ADR(3mg·kg-1ip, qod×7)可致小鼠血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(GOT)和诱导型一氧化氮合酶(iNOS)活力升高(P<0 01),同时心肌超氧化物歧化酶(SOD)活力下降而丙二醛 (MDA)含量升高 (P<0 01),线粒体水肿明显。GP( 0 75 ~3 0g·kg-1 ig, qd×15)能逆转ADR所致的上述改变,表现为剂量相关性降低血清CK、LDH、GOT和iNOS活力,增加心肌SOD活力和降低MDA含量,尤其以GP大剂量组作用明显 (P<0 05或P<0 01)。光镜和电镜结果也证实了GP的保护作用。结论　GP能拮抗阿霉素所致的小鼠中毒性心肌炎,其作用机制与增强心肌SOD活力和抗心肌脂质过氧化有关。     

复方心康口服液对大鼠心肌细胞急性缺氧/复氧损伤的保护作用

目的探讨由牛磺酸、丹参组合而成的复方心康口服液,对大鼠心肌细胞急性缺氧/复氧(A/R)损伤的保护作用。方法以1￣3d的SD大鼠的心室肌细胞为基质,利用模拟缺氧(缺血)溶液和模拟复氧(再灌)溶液,建立心肌细胞缺氧/复氧损伤模型,分为对照组(复氧组)、A/R组、心康组,分别观察3组的心肌细胞存活率、培养液中乳酸脱氢酶(LDH)活性、心肌细胞超微结构。结果A/R组与对照组相比其细胞存活率显著降低(P<0.01),心康组与A/R组相比细胞存活率明显升高(P<0.01);A/R组与对照组相比其LDH活力显著升高(P<0.01),心康组与A/R组相比LDH活力明显降低(P<0.01);对照组心肌细胞超微结构正常,A/R组心肌细胞超微结构破坏,成不可逆损伤,心康组细胞超微结构大有改善。结论复方心康口服液对大鼠心肌细胞急性A/R损伤具有显著的保护作用,表现为心肌细胞存活率明显增加、LDH活性显著降低及改善心肌细胞超微结构。由此可见,复方心康口服液作为心肌缺血、再灌注损伤治疗的辅助性用药具有较好的临床应用前景。     

安心颗粒抗心律失常及心肌缺血的作用研究

目的研究安心颗粒对心律失常和心肌缺血的改善作用。方法制备氯化钙、氯仿和乌头碱所致的小鼠心律失常模型及异丙肾上腺素（ISO）引起的小鼠心肌缺血模型,经安心颗粒治疗后,通过观察室颤发生率和心动过速的发生时间等指标评价其抗心律失常作用;通过检测血清超氧化物歧化酶（SOD）、脂质过氧化产物丙二醛（MDA）、乳酸脱氢酶（LDH）和磷酸肌酸激酶（CK）等指标评价其改善心肌缺血的作用。结果安心颗粒可降低氯仿诱发小鼠的室颤发生率;延迟氯化钙引起大鼠室性心动过速的发生时间;提高大鼠对乌头碱的耐受剂量。在ISO所致心肌缺血模型中,安心颗粒可增加SOD的活性,减少MDA的含量,降低血清LDH、CK的水平。结论安心对氯仿、氯化钙和乌头碱引起的心率失常及ISO引起的心肌缺血均有较好的改善作用。     

杏芎氯化钠注射液联合氯吡格雷治疗脑梗死的临床研究

目的探讨杏芎氯化钠注射液联合硫酸氢氯吡格雷片治疗脑梗死临床疗效。方法选取2018年10月—2019年4月在延安大学咸阳医院治疗的脑梗死患者206例,根据用药的差别分为对照组(103例)和治疗组(103例)。对照组口服硫酸氢氯吡格雷片,75 mg/次,1次/d;治疗组在对照组基础上静脉滴注杏芎氯化钠注射液,100 m L/次,1次/d。两组患者均治疗15d。观察两组患者临床疗效,同时比较治疗前后两组患者NIHSS评分、m RS评分、ESRS评分、SPI-Ⅱ评分、ADL评分、脑血流动力学,血清C反应蛋白(CPP)、白细胞介素-17(IL-17)、CXC趋化因子配体12(CXCL12)、白细胞介素-23(IL-23)、单核细胞趋化蛋白-1(MCP-1)和可溶性血管细胞黏附因子-1(s VCAM-1)水平,及血管储备功能(CVR),屏气指数(BHI)、纤维蛋白原(FIB)、全血低切黏度(LBV)、全血高切黏度(HBV)、血浆黏度(SV)和血小板聚集率(PAR)。结果治疗后,对照组和治疗组临床有效率分别为82.52%和97.09%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者NIHSS评分、m RS评分、ESRS评分和SPI-Ⅱ评分显著下降(P0.05),而ADL评分显著升高(P0.05),且治疗组患者这些评分项目明显好于对照组(P0.05)。治疗后,两组患者血清CPP、IL-17、CXCL12、IL-23、MCP-1、s VCAM-1水平均显著下降(P0.05),且治疗组比对照组下降更明显(P0.05)。治疗后,两组双侧大脑动脉Vp、Vm均显著升高(P0.05),DVp和DVm显著降低(P0.05),且治疗组改善程度最明显(P0.05)。治疗后,两组患者CVR、BHI均明显升高(P0.05),且以治疗组比对照组升高更显著(P0.05)。治疗后,两组患者FIB、LBV、HBV、SV、PAR水平均显著降低(P0.05),且治疗组这些血液流变学指标水平明显低于对照组(P0.05)。结论杏芎氯化钠注射液联合硫酸氢氯吡格雷片治疗脑梗死有利于促进患者脑神经功能恢复,提高患者生活质量、日常活动能力和降低脑血管事件发生风险。     

失笑散对异丙肾上腺素致大鼠心肌损伤的保护作用

目的探讨失笑散颗粒对异丙肾上腺素所致大鼠心肌损伤的保护作用。方法将心电图正常的Wistar健康大鼠随机分为6组（每组10只）。测定AST、CK-MB、CK、LDH、CPK、BNP、CRP、TnT。结果模型对照组大鼠的J值、AST、CK-MB、CK及LDH水平（0．199±0．132）MV、（203．43±32．81）、（80．72±27．53）、（398．37±47．26）、（400．17±128．37）U／L,明显高于空白对照组（P〈0．05）;与模型对照组相比,失笑散颗粒低剂量组能使心肌损伤大鼠的心电图J值下降值、AST、CK-MB、CK、LDH、CPK、BNP、CRP、TnT及LDH水平降低,差异无统计学意义（P〉0．05）,而中剂量组及高剂量组、阳性对照组均能使心肌损伤大鼠的心电图J值下降值、AST、CK-MB、CK、LDH、CPK、BNP、CRP、TnT水平明显明显降低（P〈0．05）。结论失笑散颗粒对异丙肾上腺素所致大鼠心肌缺血有明显的保护作用,能有效地减轻心肌损伤。     

Silymarin prevents adriamycin-induced cardiotoxicity and nephrotoxicity in rats

Adriamycin is a potent anticancer agent, its clinical use is limited for its marked cardiotoxicity and nephrotoxicity. The present study aimed to investigate the possible protective role of the natural antioxidant silymarin on ADR-induced heart and kidney toxicity. Studies were performed on four groups of rats. 1--control group, 2--silymarin group (50 mg/kg), 3--adriamycin group (10 mg/kg), 4--adriamycin+silymarin group. On the third day after ADR injection, plasma was separated for determination of LDH, CPK, cholesterol and total lipids. 30 days after ADR injection, plasma was separated for determination of creatinine and urea levels. Frozen heart specimens (72 h) and frozen kidney specimens (30days) were used for estimation of lipid peroxides and GSH contents. Histopathological examinations of heart and kidney sections were also done. Pretreatment of ADR-treated rats with silymarin resulted in a significant decrease in the plasma CPK, LDH, creatinine and urea. On the other hand silymarin pretreatment did not change ADR-induced hyperlipidemia. Silymarin pretreatment significantly decreased the myocardial MDA contents. In addition, silymarin pretreatment normalized renal tissue contents of MDA and GSH. Histopathological examination of heart and kidney sections revealed that ADR caused only mild myocardial injury in silymarin pretreated rats. Also, silymarin pretreatment inhibited ADR-induced renal tubular damage in rats. These results have suggested that, silymarin ameliorated ADR-induced cardiotoxicity and protected against ADR-induced nephrotoxicity in male albino rats. The mechanisms of silymarin induced protection against ADR-induced toxicities were proved to be due to inhibition of lipid peroxidation and protection against GSH depletion.     

Study of the pharmacological effect of the bile salt, sodium scymnol sulfate, from Rhizoprionodon acutus. III. Protective effect of scymnol against vascular endothelial cell damage in a rat peripheral arterial occlusion model.

The prophylactic action of scymnol in a rat peripheral arterial occlusion model, involving injection of 5% lactic acid into the femoral artery, was investigated. Increases in serum lactate dehydrogenase (LDH), glutamic oxaloacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) activities and in plasma levels of thrombin and antithrombin III complex (TAT) were observed in this model 3 h after injection of lactic acid. Changes in LDH activity were characterized by increases in isozymes LDH4 and LDH5 and an elevated LDH4/LDH5 ratio. The ratio of the LDH4 to LDH5 increments was similar to that seen in a rat endothelial cell culture. Oral preadministration of scymnol had a preventive effect on the development of lesions in this model. It significantly reduced the LDH4 and LDH5 activity, the LDH4/LDH5 ratio and the TAT levels dose-dependently over the range 1, 3 or 10 mg/kg, compared with the values in control rats. However, its administration after lactic acid injection, or to sham-operated rats was ineffective, even at a dose of 10 mg/kg. The effects of scymnol were also compared with those of ticlopidine and argatroban. The findings show that scymnol may be useful in preventing thrombotic peripheral arterial occlusive disorders and that it potently protects endothelial cells against lactic acidosis in this model.     

荭叶心通软胶囊对小鼠耐缺氧及体外培养心肌细胞的影响

目的观察荭叶心通软胶囊对小鼠耐缺氧及体外培养心肌细胞的影响。方法夹闭小鼠气管,以不同剂量的荭叶心通软胶囊与普萘诺尔做对照,观察给药后小鼠缺氧心跳停止时间;离体培养大鼠乳鼠原代心肌细胞,以不同剂量的荭叶心通软胶囊与香丹注射液做对照,检测给药后心肌细胞A570和培养上清液中LDH活力。结果荭叶心通软胶囊高、中剂量组能明显延长小鼠气管结扎的心跳时间,增加小鼠心脏耐缺氧能力。荭叶心通软胶囊高剂量组可明显提高心肌细胞A570,降低培养上清液LDH的活力。结论荭叶心通软胶囊具有改善小鼠耐缺氧的作用,对NaCN诱导心肌细胞损伤具有一定的保护作用。     

PNU282987对异丙肾上腺素所致小鼠心脏重塑的保护作用

目的通过建立异丙肾上腺素所致小鼠心脏重塑模型,观察PNU282987保护心脏的作用。方法连续7 d皮下注射异丙肾上腺素(ISO),诱导小鼠心脏重塑模型,同时腹腔给予PNU282987,检测小鼠心脏重量指数、血清乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性,观察心肌病理形态学的改变;检测心肌组织中超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,通过Western blot测定诱导型一氧化氮合酶(iNOS)的表达。结果与正常对照组相比,异丙肾上腺素组心脏重量指数增加,血清LDH和CK水平显著升高,心肌SOD活性下降,MDA含量增加,心肌组织中iNOS蛋白表达增加;与模型组比较,PNU282987可显著降低心脏重量指数、血清LDH和CK水平,增加心肌SOD活性,降低心肌MDA含量,下调iNOS表达。结论 PNU282987可能通过清除氧自由基,降低iNOS的表达,保护异丙肾上腺素导致的小鼠心脏重塑。     

LD50 values and serum biochemical changes induced by T-2 toxin in rats and rabbits

Experiments were conducted to study the acute and subacute effects of intramuscularly injected T-2 toxin in rats and rabbits. The LD50 values of T-2 toxin were 0.85 ± 0.03 and 1.10 ± 0.08 mg/kg body wt in rats and rabbits, respectively. The intoxication was characterized by a consistent decrease in serum alkaline phosphatase (ALP) activity following either a single injection of 0.5, 0.6, or 0.9 mg/kg T-2 toxin in rats or daily injections of 0.2 mg/kg T-2 toxin for 10 days in rats and rabbits. Significant increases in bromosulfalein (BSP) retention and ALP activity were also observed in rabbits 24 hr following a single injection of 0.6 mg/kg T-2 toxin. The results indicated that the hepatobiliary system is a major target organ for T-2 toxin. Alterations in the activity of lactate dehydrogenase (LDH) and creatine kinase (CK) and in the hematocrit values were also observed.     

低分子肝素钙对心肌缺血损伤模型大鼠心肌保护作用的研究

目的:研究低分子肝素钙(LHC)对心肌缺血损伤模型大鼠心肌的保护作用及其机制。方法:取60只大鼠随机分为正常对照组、模型对照组、丹参注射液阳性对照组和LHC高、中、低剂量组(n=10),给予相应药物后腹腔注射异丙肾上腺素建立大鼠心肌缺血模型,之后观察大鼠体表心电图(ECG),测定血清心肌酶(LDH、CK)、血清超氧化物歧化酶(SOD)活性和丙二醛(MDA)的含量。结果:与模型对照组比较,LHC可明显改善心肌缺血大鼠ECG中S-T段偏移的幅度,显著降低血清LDH、CK、MDA的活性或含量(P<0.01,P<0.05),同时可提高血清SOD的活性(P<0.05)。结论:LHC可能通过改善抗氧化酶等指标活性使心肌坏死程度减轻。     

大蒜多糖对阿霉素所致心肌细胞损伤的保护作用

目的观察大蒜多糖(GP)对阿霉素(ADR)中毒心肌细胞的保护作用并探讨其机制。方法采用0~2 d SD乳鼠心肌细胞做原代培养,复制ADR损伤心肌细胞模型,测定上清液及细胞中多项生化指标,并运用MTT比色法、流式细胞仪检测凋亡细胞。结果ADR(终浓度为1 mg.L-1)可致上清液肌酸激酶(CK)、乳酸脱氢酶(LDH)、谷草转氨酶(GOT)释放量增加(P<0.01),同时细胞超氧化物歧化酶(SOD)活力下降而丙二醛(MDA)含量升高(P<0.01),GP(25~100 mg.L-1)可呈浓度依赖性地降低CK、LDH、GOT活力,增加细胞SOD活力和降低MDA含量,尤其以GP大剂量组作用明显(P<0.05或P<0.01)。流式细胞仪检测GP能降低心肌细胞凋亡率,证实了GP的保护作用。结论GP能够拮抗ADR引起的自由基脂质过氧化,从而保护心肌细胞。     

急性低钾血症与房室传导阻滞相关性研究

目的探讨低钾血症与房室传导阻滞的关系。方法对93例病程不超过48h的低钾血症患者进行回顾性分析,对其中11例房室传导阻滞病例与随机选取的11例心电图正常的低钾血症病例,对心肌酶包括谷草转氨酶(glutamic oxaloacetic transaminase,AST)、乳酸脱氢酶(lactic dehydrogenase,LDH)和肌酸激酶(creatine kinase,CK)及血清钾水平进行对比分析。结果血清钾水平2组无明显差异(P>0.05);合并房室传导阻滞组与对照组AST、CK无明显统计学差异(P>0.05),心电图正常组LDH高于合并房室传导阻滞组(P<0.05)。结论急性低钾血症时,血钾降低水平、心肌酶改变与是否引起房室传导阻滞与无明显关系。     

The protective effect of glutathione administration on adriamycin-induced acute cardiac toxicity in rats.

Adriamycin (ADR) is a potent antitumor antibiotic drug known to cause severe cardiac toxicity. Although ADR generates free radicals, the role of these radicals in the development of cardiac toxicity is still not well understood. In the present study, we evaluated the effect of glutathione (GSH) supplementation or depletion on ADR-induced cardiotoxicity in male Wistar rats. Cardiac toxicity was induced by a single intraperitoneal injection of ADR (20 mg kg(-1)) and manifested by an increase in heart rate, blood pressure elevation, and increased serum creatine kinase (CK) and lactate dehydrogenase (LDH). The extent of lipoprotein oxidation, lipid peroxide measured as malondialdhye (MDA), total homocysteine (tHcy), lipid profile, and atherogenic index were markedly elevated, whereas cardiac GSH content was dramatically decreased in ADR rats. Pre- and co-treatment of ADR rats with GSH (5 mm kg(-1)) (ADR +GSH) markedly reduced the levels of CK, LDH, lipoprotein oxidation susceptibility, cardiac MDA, tHcy and atherogenic index, and elevated GSH levels in cardiac tissues. In contrast, GSH depletion through administration of l-buthionine-(S,R)-sulfoximine (BSO) (15 mm kg(-1)) before and after ADR injection (ADR +BSO) greatly exacerbated ADR cardiotoxicity compared to the control and ADR groups. Finally, there were also severe cardiac histopathological changes in ADR and ADR +BSO groups, which were nearly restored by GSH treatment. These results suggest that GSH inhibits ADR cardiotoxicity and might serve as a novel combination with ADR to limit free radical-mediated organ injury.     

<Emphasis Type="Italic">Phyllanthus maderaspatensis</Emphasis>, a dietary supplement for the amelioration of adriamycin-induced toxicity and oxidative stress in mice

The effect of ethanol extract of Phyllanthus maderaspatensis (PME), a popular south Indian dietary supplement, was studied for its chemoprotective property on adriamycin (ADR)-induced toxicity and oxidative stress in mice. Adriamycin toxicity was evaluated biochemically by measuring the serum concentration of lactate dehydrogenase (LDH) and creatinine phosphokinase (CPK). Genotoxicity was evaluated by measuring the frequency of micronucleated polychromatic erythrocytes (MNPCEs) in bone marrow cells. Oxidative stress in the heart tissue was estimated by measuring the glutathione (GSH) levels in the homogenate. The treatment of mice with different doses of PME (400 mg/kg and 600 mg/kg body weight, p.o.,) for 7 days before the administration of a single i.p. dose of ADR (15 mg/kg) exhibited significant protection in a dose-dependent manner. The results clearly indicate that PME has a protective effect against ADR-induced toxicity, as revealed by the decrease in the concentrations of LDH, CPK, and the frequency of MNPCEs. The increased levels of GSH are indicative of the antioxidant property of PME.     

转化糖注射液对住院患者血糖及胰岛素水平的影响

目的:观察转化糖注射液对各种需要静脉补充能量及体液的住院患者血糖、胰岛素水平的影响,并评价其安全性。方法:采用随机、双盲、对照的多中心临床试验。共入选病例240例,试验组(120例)静脉滴注转化糖注射液500ml/d,对照组(120例)静脉滴注葡萄糖注射液500ml/d,疗程均为3天。给药期间检测患者的血糖、胰岛素,给药前后作心电图、血尿常规、肝肾功能及血尿酸、电解质等检查,密切观察患者的临床症状及体征变化。结果:转化糖组的血糖及胰岛素水平的波动小于葡萄糖组(P<0.05),试验前后的生命体征、血尿常规、肝肾功能、电解质、心电图等均未出现与药物相关的异常变化。结论:转化糖对血糖及胰岛素水平的影响小于葡萄糖,其安全性与葡萄糖注射液相当。     

吴茱萸次碱对实验动物急性心肌缺血损伤的保护作用

目的探讨吴茱萸次碱(Rut)对实验动物急性心肌缺血损伤的保护作用。方法采用垂体后叶素及异丙肾上腺素致小鼠急性心肌缺血模型,检测血清中乳酸脱氢酶(LDH)、肌酸激酶(CK)的活性。进一步采用大鼠冠状动脉结扎模型,检测血流动力学指标及血清LDH、CK、超氧化物歧化酶(SOD)的活性及丙二醛(MDA)的含量。结果与模型组相比,Rut组能降低垂体后叶素及异丙肾上腺素所致小鼠血清LDH及CK的升高(P<0.05)。在大鼠冠状动脉结扎实验中,与模型组相比,Rut组能改善结扎大鼠血流动力学指标的变化,血清中LDH、CK的酶活力及MDA的含量下降,SOD活力升高(P<0.05)。结论 Rut对实验动物急性心肌缺血有一定的保护作用。     

Morin reduce uric acid level in hyperuricemia mice

OBJECTIVE To explore morin's effect on hyperuricemia mice. METHODS Mice were grouped as control, model, morin low dose, middle dose, high dose,allopurinol, benzbromarone. Hyperuricemia model was built by 300 mg · kg~(-1) potassium oxonate intraperitoneal injection. After model built, administrated morin two weeks and sampled serum, kidneys, ileum and liver. Assay UA, BUN, CRE, AST, ALT, TG, CHO, ALB, HDL, LDL by Biochemical analyzer. RESULTS Morin groups can reduce the serum uric acid. Compared with allopurinol,morin have less BUN level and CRE level in serum. Morin can reduce ALT level and high dose of morin group significantly reduce LDH level. CONCLUSION morin can reduce the serum uric acid on hyperuricemia mice, meanwhile, has liver and kidneys protective effects in some degrees.     

Prevention of silybin of phalloidin-induced acute hepatoxicity

In mice, the acute hermorrhagic necrosis of the liver induced by phalloidin was prevented by treatment with silybin, a plant compound isolated from Silybum marianum L. Gaertn. By electron microscopy, the first changes induced by the toxin were detected at the level of the hepatocytic plasmalemma and were followed by the development of cytoplasmic vacuoles containing blood-derived material. These morphologic changes can be correlated with enhancement of serum activities of glutamic pyruvic and oxaloacetic transaminases and of lysosomal hydrolases. Pretreatment with a single dose of silybin completely abolished the morphologic changes induced by the toxin and significantly decreased the activities of serum enzymes. Silybin when given alone did not result in changes of serum enzymes activities or of hepatocytic ultrastructure.