甘遂半夏汤中甘遂甘草反药组合加减应用对腹水大鼠CYP450酶的影响

目的：从细胞色素(CY)P450酶的角度,以甘遂半夏汤复方为载体,探究腹水病理模型下甘遂甘草配伍“反”与“不反”。方法：150只Wistar大鼠随机分为正常组、模型组、甘遂半夏汤全方组(5.68 g·kg^-1·d^-1)、甘遂半夏汤全方去甘遂组(5.57 g·kg^-1·d^-1)、甘遂半夏汤全方去甘草组(4.01 g·kg^-1·d^-1)、甘遂半夏汤全方去甘草甘遂组(3.90 g·kg^-1·d^-1),其中甘遂1.1 g、法半夏9 g、白芍15 g、炙甘草16.7 g、蜂蜜15 g,每组25只,除正常组外,其余各组大鼠腹腔注射Walker-256细胞复制大鼠癌性腹水模型,正常组、模型组灌胃蒸馏水,其余给药组灌胃相应药液,连续给药7 d;用高效液相色谱法(HPLC)检测探针药物浓度,通过计算代谢率来测定CYP450酶活性;用实时荧光定量聚合酶链式反应(Real-time PCR)测定CYP450酶基因表达;用蛋白免疫印迹法...     

姜酚对小鼠肝药酶活性的影响

目的:研究姜酚对小鼠肝脏细胞色素氧化酶P450(CYP450)含量及其亚型CYP2E1与CYP3A活性的影响。方法:小鼠口服给药姜酚(200,100,50 mg.kg-1.d-1),5 d后钙沉淀法制备肝微粒体,测定并考察姜酚对小鼠肝重、微粒体蛋白、CYP450及CYPb5含量的影响;氨基比林法和红霉素法测定肝微粒体CYP亚型CYP2E1与CYP3A的活性。结果:姜酚高、中、低剂量(200,100,50 mg.kg-1.d-1)对小鼠肝重、蛋白含量无影响,能显著降低CYP450的含量以及增加CYPb5的含量(P<0.01);3种剂量姜酚均可抑制CYP2E1的活性(P<0.05),且随着剂量增加抑制作用增强,高剂量姜酚可以抑制CYP3A的活性(P<0.05)。结论:姜酚对小鼠CYP450含量及亚型CYP2E1,CYP3A活性有抑制作用,抑制程度与剂量有关。     

五子衍宗丸对雷公藤多苷致肾病综合征雄鼠生殖损伤的机制研究

目的：观察五子衍宗丸干预肾病综合征SD大鼠对生精细胞T型Ca²⁺通道及顶体酶PPEF1活性的影响及作用机制。方法：按照随机数字表法将70只SD大鼠分为空白组(蒸馏水1 mL灌胃)、肾病模型组(蒸馏水1 mL灌胃)、肾病模型+雷公藤多苷组(雷公藤多苷0.04 mg·kg^-1·d^-1灌胃)、肾病模型+五子衍宗丸组(五子衍宗丸1.07 g·kg^-1·d^-1灌胃)、肾病模型+雷公藤多苷+低剂量五子衍宗丸组(雷公藤多苷0.04 mg·kg^-1·d^-1与五子衍宗丸0.54 g·kg^-1·d^-1同时灌胃)、肾病模型+雷公藤多苷+中剂量五子衍宗丸组(雷公藤多苷0.04 mg·kg^-1·d^-1与五子衍宗丸1.07 g·kg^-1·d^-1同时灌胃)、肾病模型+雷公藤多苷+高剂量五子衍宗丸组(雷公藤多苷0.04 mg·kg     

何首乌、制何首乌与茯苓配伍对大鼠肝微粒体细胞色素P450的影响

目的:研究何首乌、制何首乌以及分别配伍不同剂量茯苓对大鼠肝脏微粒体细胞色素P450酶(CYP450)的影响。方法:将大鼠分为7组,每日灌胃主药30g·kg-1,连续给药90d,测定大鼠CYP450的含量。结果:给药组与对照组比较,何首乌A组、何首乌B量组对大鼠肝微粒体CYP450有显著性升高作用(P<0.05);何首乌C组对其有升高作用,但不具统计学意义。制何首乌A、B、C各组对大鼠肝微粒体CYP450均无显著性影响。结论:何首乌、何首乌配伍大剂量茯苓能够增加大鼠肝微粒体CYP450含量,制何首乌各给药组对其影响不显著。     

甘草减轻雷公藤多苷片所致肝损伤的作用机制

目的：探究肝脏药物代谢关键酶细胞色素P4502D6(CYP2D6)、细胞色素P4503A4(CYP3A4)在甘草水提物对急性肝损伤发挥保护作用的分子机制。方法：将健康雄性昆明种小鼠分为正常组、模型组、甘草水提物低、中、高剂量组(5、10、15 g·kg^-1·d^-1)及阳性药甘草酸二铵组(75 mg·kg^-1·d^-1),每组10只。以预防给药1周后采用雷公藤多苷片270 mg·kg^-1单次灌胃诱导急性肝损伤模型,作用18 h后采集样本。采用苏木素-伊红(HE)染色观察肝脏病理变化;生化法检测血清中肝功能指标丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、γ-谷氨酰转肽酶(γ-GT)、碱性磷酸酶(ALP)和总胆红素(TBIL)的含量及肝细胞氧化应激指标丙二醛(MDA)、超氧化物歧化酶(SOD)的水平;实时荧光定量聚合酶链式反应(Real-time PCR)和蛋白免疫印迹法(Western blot)分别检测肝脏药物代谢关键酶CYP2D6、CYP3A4的mRNA及蛋白表达...     

基于Fas/FasL介导的凋亡信号通路研究通管方对输卵管炎性不孕模型大鼠的作用机制

目的：探讨通管方对输卵管炎性不孕(SI)模型大鼠输卵管组织中Fas/FasL通路的影响。方法：采用经阴道内接种混合菌液的方法,建立输卵管炎性不孕大鼠模型。造模后,77只SD雌性大鼠随机分成空白组、假手术组、模型组、妇可靖胶囊组(0.29 g·kg^-1·d^-1)、通管方低剂量组(7.515 g·kg^-1·d^-1)、通管方中剂量组(15.03 g·kg^-1·d^-1)、通管方高剂量组(30.06 g·kg^-1·d^-1),各组大鼠分别灌胃给药28 d后处死并取材。采用蛋白免疫印迹法(WB)检测SI模型大鼠输卵管组织中Fas、FasL蛋白及Caspase-1的表达水平,酶联免疫吸附法(ELISA)检测SI模型大鼠血清IL-4、IL-10、Caspase-1的表达变化。结果：与空白组比较,模型组血清中IL-4和IL-10的水平均明显降低,血清和输卵管组织中的Caspase-1水平明显升高(P<0.01);与模型组比较,...     

基于肠道菌群与肠道代谢探究脉络舒通丸对大鼠股骨骨折引起的后肢肿胀的治疗作用及机制

探讨脉络舒通丸对大鼠股骨骨折引起的后肢肿胀的保护作用及其潜在机制。将大鼠随机分为假手术组、模型组、脉络舒通丸(MLST)低剂量组(1.8 g·kg^-1·d^-1)、MLST高剂量组(3.6 g·kg^-1·d^-1)和阳性药组(迈之灵片60 mg·kg^-1·d^-1)。假手术组暴露股骨后缝合伤口，其余4组均进行机械性损伤造成股骨骨折，于造模前7 d及造模后5 d对各给药组给予灌胃给药，假手术组、模型组给予等剂量蒸馏水灌胃。采用苏木精-伊红(hematoxylin-eosin, HE)染色检测大鼠后肢肌肉组织的病理损伤，并测量其后肢肿胀度。酶联免疫吸附测定(enzyme-linked immunosorbent assay, ELISA)试剂盒检测各组大鼠血清中白细胞介素-6(interleukin-6, IL-6)、白细胞介素-1β(interleukin-1β, IL-1β)、肿瘤坏死因子-α(tumor necrosis factor-α, TNF-α)的水平...     

首乌藤联合黄芪对刀豆蛋白A诱导的小鼠免疫性肝损伤的影响

目的 观察中药首乌藤联合应用黄芪对刀豆蛋白A(ConA)诱导的免疫性肝损伤模型小鼠的影响。方法 健康ICR小鼠(SPF级)70只,随机分为正常组(等量0.9%NaCl溶液)、模型组(等量0.9%NaCl溶液)、正常+低剂量首乌藤组(首乌藤药液2 g·kg^-1·d^-1)、正常+高剂量首乌藤组(首乌藤药液6 g·kg^-1·d^-1)、模型+低剂量首乌藤组(首乌藤药液2 g·kg^-1·d^-1)、模型+高剂量首乌藤组(首乌藤药液6 g·kg^-1·d^-1)及模型+高剂量首乌藤+黄芪组(首乌藤药液2 g·kg^-1·d^-1+黄芪药液6 g·kg^-1·d^-1),每组10只。各组均每日灌胃1次,连续10 d。末次灌胃后模型组、模型+低剂量首乌藤组、模型+高剂量首乌藤组、模型+高剂量首乌藤+黄芪组予ConA 10 mg·kg^-1     

基于Nrf2/Keap1信号通路探讨人参肽对D-半乳糖联合AlCl3衰老模型小鼠的作用

目的：基于核因子E2相关因子2(Nrf2)/Kelch样环氧氯丙烷相关蛋白-1(Keap1)信号通路探讨人参肽对D-半乳糖(D-gal)联合AlCl3衰老模型小鼠的影响及分子机制。方法：将50只KM小鼠随机分为对照组、模型组、阳性药组、人参肽低剂量组、人参肽高剂量组,每组10只,阳性药组给予参茸片286.3 mg·kg^-1·d^-1;人参肽低、高剂量组分别给予人参肽17.5 mg·kg^-1·d^-1、35 mg·kg^-1·d^-1,预给药7 d后,除对照组外,其余各组小鼠均给予500 mg·kg^-1·d^-1 D-gal皮下注射与70 mg·kg^-1·d^-1 AlCl3灌胃30 d联合给药制备衰老模型,应用PCR检测各组小鼠鼠尾组织早老素-1(PS1)的基因表达水平验证模型是否制备成功;通过爬杆实验、负重游泳实验测试小鼠协调能力、抗疲劳能力;应用生化法检测小鼠肝组织中超氧化物歧...     

丹参酚酸A对大鼠肝微粒体细胞色素P450酶系的影响

目的:研究丹参酚酸A对大鼠肝微粒体细胞色素P450和细胞色素b_5含量以及CYP1A2和CYP2E1活性的影响.方法:将大鼠分成溶剂对照组和丹参酚酸A给药组,每组10只,雌雄各半,丹参酚酸A给药组尾静脉注射给予丹参酚酸A 20 mg·kg~(-1)·d~(-1),连续给药5 d;溶剂对照组给予相同剂量的溶剂,紫外分光光度法测定大鼠肝微粒体细胞色素P450和细胞色素b_5含量;探针底物法评价CYP1A2和CYP2E1的活性.结果:丹参酚酸A尾静脉注射连续给药5 d后,大鼠细胞色素P450和细胞色素b_5含量与对照组比较均无显著性差异;CYP1A2和CYP2E1的活性与对照组比较也无显著性差异.结论:丹参酚酸A对CYP1A2和CYP2E1没有诱导或抑制作用,与经过CYP1A2和CYP2E1代谢的药物发生相互作用的可能性较小.     

黄连温胆汤对IGT大鼠炎症反应与肝细胞焦亡的影响

目的:探讨高脂饮食诱导糖耐量低减(IGT)大鼠是否存在炎症反应与细胞焦亡及黄连温胆汤对其干预作用.方法:健康雄性SD大鼠予45％脂肪含量饲料喂养20周复制IGT模型.将符合模型标准的大鼠随机分为3组,每组10只,另取10只空白鼠作为正常组.黄连温胆汤组予7.8 g·kg-1·d-1复方水煎液,阳性药组予盐酸二甲双胍水溶...     

艾迪注射液对DEN诱导型肝癌大鼠体内细胞色素P450酶表达的影响

目的:观察艾迪注射液(AD)对二乙基亚硝胺(DEN)化学诱导的原发性肝癌(HCC)大鼠体内细胞色素P450(CYP450)4种亚型酶CYP1A2,CYP2E1,CYP3A2,CYP2C11 mRNA和蛋白表达的影响.方法:健康SD雄大鼠随机选取3只作为空白组,余下大鼠采用DEN间断性诱导原发性肝癌大鼠模型,模型成功后随...     

逍遥散加减方对高催乳素血症大鼠卵巢自分泌及旁分泌机制的影响

目的:探讨逍遥散加减方对高催乳素血症大鼠模型卵巢自分泌及旁分泌机制的影响.方法:采用腹腔注射甲氧氯普胺制成高催乳血症大鼠模型,随机分为6组:空白组、模型组、逍遥散加减方高、中、低剂量组(分别予以逍遥散加减方60、30、15g·kg-1·d-1)、溴隐亭组0.001g·kg-1·d-1,药物治疗30d后通过免疫组化检测大...     

芍药汤对大肠湿热型溃疡性结肠炎大鼠结肠组织中CD14，FADD，Caspase-8表达的影响

目的:观察芍药汤对大肠湿热型溃疡性结肠炎(UC)模型大鼠血清中细胞黏附分子-1(ICAM-1),转化生长因子-β1(TGF-β1)含量及病灶结肠组织中白细胞分化抗原14(CD14),Fas相关死亡结构域蛋白(FADD)与天冬半胱氨酸蛋白酶-8(Caspase-8)mRNA及蛋白表达的影响。方法:将SPF级Wistar大鼠80只随机分为正常组10只、造模组70只,采用病证结合的方式复制大肠湿热型UC大鼠,即高脂高糖辛辣饮食+2,4-二硝基苯磺酸(DNBS)结合乙醇复合法造模,造模成功后,按随机数字表法将造模组分为模型组、柳氮磺砒啶(SASP)组及芍药汤低、中、高剂量组,每组14只,给予柳氮磺嘧啶0.2 g·kg^-1·d^-1,芍药汤低、中、高剂量(6,12,24 g·kg^-1·d^-1)灌胃,正常组及模型组给予等体积生理盐水灌胃,连续21 d。采用酶联免疫吸附测定(ELISA)法检测血清ICAM-1,TGF-β1含量,实时荧光定量聚合酶链式反应(Real-time PCR)检测结肠组织CD14,FADD,Caspase-8 mRNA表达,蛋白免疫印迹法(Western blot)检测结肠组织CD14,FADD,Caspase-8蛋白表达。结果:与正常组比较,模型组大鼠血清中ICAM-1含量明显升高,TGF-β1含量明显降低(P<0.05);CD14,FADD,Caspase-8 mRNA及蛋白相对表达量明显升高(P<0.05)。与模型组比较,芍药汤中、高剂量组及SASP组大鼠血清中ICAM-1含量明显降低,而芍药汤低、中、高剂量组及SASP组大鼠血清中TGF-β1含量明显升高(P<0.05);各干预组CD14,FADD,Caspase-8 mRNA及蛋白表达量明显降低(P<0.05),并以芍药汤高剂量组及SASP组更为明显。结论:芍药汤对大肠湿热型UC大鼠具有一定干预作用,其机制可能与抑制CD14,FADD及Caspase-8 mRNA及蛋白的表达有关。     

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??OBJECTIVE To investigate the influence and mechanism of different doses of Yangxinshi on infarction region angiogenesis of Wistar rats after acute myocardial infarction. METHODS Sixty healthy male Wistar rats were randomly divided into five groups, named as follow:group A: rosuvastatin group (0.75 mg??kg^-1??d^-1), group B: high-dose Yangxinshi(0.27 g??kg^-1??d^-1),group C:mid-dose Yangxinshi group (0.18 g??kg^-1??d^-1),group D: Low-dose Yangxinshi group (0.09 g??kg^-1??d^-1),group E:saline control group. A, B, C, D group was respectively given the drug by gavage, group E received normal saline by gavage. The models of acute myocardial infarction can be established in the forth week . After continued drugs for 4 weeks, rats were killed before detected blood biochemicalindexes such as blood lipids, liver and kidney function. Myocardial tissue was sliced and stained infarcted myocardium by HE to observe the pathological changes, also extract ischemic and infarct myocardium tissue protein and test VEGF protein expression with immunohistochemistry. RESULTS Myocardial tissue HE staining were observed a lot of survival island cardiomyocytes and neonatal thin-walled capillaries in four treatment groups , however,control group exist less normal cardiomyocytes and capillaries mainly disappear. Immunohistochemistry RESULTS showed high-doses of Yangxinshi group express higher VEGF protein compared with mid-dose group, low-dose group and control group, the difference was statistically significant (P<0.05), VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference was statistically significant (P<0.05). CONCLUSION Yangxinshi promote production of VEGF protein and angiogenesis of ischemic myocardium ,in addition its role and its dose is positive correlated. VEGF protein expression was significantly increased the in mid-dose and high-dose Yangxinshi groups than rosuvastatin group, the difference is statistically significant (P<0.05).     

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??OBJECTIVE To investigate the preventive effects of coenzyme Q10 on cortical bone in cyclophosphamide-treated rats and compare CoQ10 with alendronate sodium. METHODS Thirty-two three-month-old SPF and SD male rats were randomly divided into 4 groups (n=8 per group). Group 1 was treated with vehicle as the control group (CON group).Other groups were treated with cyclophosphamide (4.5 mg??kg^-1??d^-1) first, and then vehicle (CTX group), alendronate sodium (ALD 1 mg??kg^-1??d^-1) and CoQ10(30 mg??kg^-1??d^-1) once a day for 15 d. At the experimental endpoint, The static and dynamic parameters of left tibia bone grinding by the bone histomorphometry and took the right femur bone biomechanical testing were observated. RESULTS From bone histomorphometry parameters, cyclophosphamide can inhibit bone formation which make rat cortical bone thinning, bone marrow cavity to expand; reduced bone formation. Coenzyme Q10 can effectively promote bone formation, inhibit bone loss in rats by cyclophosphamide, the effect is better than the positive drug alendronate sodium. Compared with the CON group, biomechanical properties of maximal strength, break strength, break strain and toughness index were decreased significantly, while modulus of rigidity was increased significantly in the CTX group. Compared with the CTX group, the ALD group, only several parameters of the biomechanical properties were significantly improved. In contrast, in the CoQ10 group, the biomechanical properties were significantly improved. CONCLUSION CoQ10 (30 mg??kg^-1??d^-1) on the microstructure of CTX rat tibia bone repair capacity better, and the ability to repair bone mass and reduce the risk of hip fracture is also superior ALD.     

The effect of a strongly basic alkaloidal fraction of Rhazya stricta,a traditional medicinal plant,on cytochrome P450-mediated metabolism of theophylline in mice

The strongly basic alkaloidal fraction of the traditional medicinal plant Rhazya stricta (RS) was given orally to mice, in a single dose of 10 mg/kg (group 1) or, twice daily for 3 days at the same dose (group 2). A third group (control) received normal saline. Liver homogenates from all animals were used to assess the microsomal activity of cytochrome P450 and its isoforms as well as its catalytic activity (using theophylline as a substrate). RS alkaloidal fraction had no significant effect on the total amount of microsomal cytochrome P450, but it caused a significant increase in the cytochrome P450 isoforms CYPs 1A1 and 1A2. It also significantly increased the concentrations of some metabolites of theophylline. These results suggest that RS has the potential to interact with other drugs that are biotransformed by cytochrome P450, when given concomitantly with it.     

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??OBJECTIVE To explore whether QSC can have cardioprotective efficacy after myocardial infarction(MI),we design this experiment in a preclinical model of myocardial infarction in rats. METHODS Four weeks after left anterior descending coronary artery ligation, rats received either intragastric administration of QSC,or the same volume of saline.Male SD rats were given the ligation of anterior descending coronary artery. After 4 weeks,42 male rats were chosen and randomly divided into 3 groups. The model group(normal saline solution for 4w, n=14), low-dose control group(5??10⁴ mg??kg^-1??d^-1 of drug QSC, for 4w, n=14), and QSC moderate dose group(10??10⁴ mg??kg^-1??d^-1 of QSC for 4w,n=14). The sham-operation group(n=16) was only given treatment of chest-open without ligation of anterior descending coronary artery,divided into 2 groups,the Sham-group(normal saline solution for 4w,n=8)and Sham+QSC group(5??10⁴ mg??kg^-1??d^-1 of drug QSC,for 4w,n=8).Cardiac function was assessed echo cardio-graphically.Angiogenesis and apoptosis were detected using histology and Western blot methods four weeks after QSC therapy. RESULTS Reductions in infarction area and scar collagen content in MI+QSC group were observed in the infarct region compared with the saline control and MI+QSCL group. QSC also improved cardiac function after treatment. QSC significantly decreased apoptosis relative to control group, evidenced by influencing the expression of Bcl-2, Bax, cytochrom C and caspase-3 in the myocardial infarction. Meanwhile, angiogenesis in the infarctive regions were significantly enhanced relative to control group, evidenced by increased density of a-smooth muscle actin and CD31 positive vessels respectively. Similarly, the mRNA expressions of VEGF and HIF-1?? were up-regulated.Additionally. OSC involvement also increased the phosphorylation of AKT and down-regulated the phosphorylation of MEK/ERK. CONCLUSION There is no significant difference between QSC low-dose group and the model group, but QSC moderate dose group can improve cardiac function in rats after MI, the underlying mechanism of which can be explained by increasing angiogenesis,reducing apoptosis partially via the activation of AKT signaling pathway and inhibition of phosphorylation of MEK/ERK.     

养心定悸胶囊对异丙肾上腺素诱导SD大鼠缺血性心律失常的拮抗作用及机制

目的探讨养心定悸胶囊对缺血性心律失常的拮抗作用及机制。方法 60只健康雄性SD大鼠随机分为6组:对照组,模型组,普萘洛尔组和养心定悸低、中、高剂量组。异丙肾上腺素(isoproterenol, ISO)注射诱导缺血性心律失常。各组大鼠灌胃给药,1次/d,连续7 d,普萘洛尔组给予普萘洛尔15 mg·kg^-1·d^-1;养心定悸低、中、高剂量组分别给予养心定悸胶囊0.5、1、2 g·kg^-1·d^-1;对照组和模型组给予0.9%氯化钠溶液。采用BL-420F系统记录大鼠心电图变化;采用HE、Masson、TTC染色观察心肌组织病理损伤情况;采用ELISA测血清肌钙蛋白(cTnI)、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、白细胞介素-1β(IL-1β)水平;采用自动生化仪测血清丙二醛(MDA)、超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)水平。结果与对照组比较,模型组大鼠室早及室速频发,心电图ST段抬高,心律失常评分增加(P<0.01);心脏指数(HWI)增加(P<0.01);心肌组织缺血损伤及病理损伤明显;氧化应激指标变化明显(P<0.01);血清炎症因子水平多升高(P<0.01或P<0.05)。与模型组比较,普萘洛尔组及养心定悸组大鼠发生室早及室速时间延迟、频次降低,心电图ST段抬高幅度减轻,心律失常评分降低(P<0.05);HWI降低(P<0.01);心肌组织病理损伤减轻;缺血损伤面积减小;血清cTnI降低(P<0.01或P<0.05);氧化应激状态改善(MDA水平降低而SOD、GSH升高)(P<0.01或P<0.05);血清炎症因子(TNF-α、IL-6等)水平降低(P<0.01或P<0.05)。结论养心定悸胶囊可以有效改善ISO诱导大鼠缺血性心律失常,其作用机制与其抑制氧化应激和炎症反应从而减轻心肌细胞损伤有关。     

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??OBJECTIVE To discuss the effect and mechanism of cinepazide maleate (CM) on myocardial injured rats induced by isoproterenol (Iso). METHODS Fifty male and female rats were divided into normal group, model group, the low and the high dose group of the CM, and captopril (Cap)positive control group. The rat model of myocardial injury was established by subcutaneous injection of Iso (5 mg??kg^-1??d^-1)for 7 d, rats in treatment group were given intraperitoneal injection of CM on the second day (1.5,3 mg??kg^-1??d^-1), rats in positive control group were given intragastric administration of Cap(10 mg??kg^-1??d^-1), and rats in normal group and model group were given intraperitoneal injection of normal saline in the same volume, for 14 d. The rats in each group were tested before and after treatment by three times of running endurance test. After stopping drug all rats were anesthetized for measuring the electrocardiogram (ECG), then taken blood for measuring the activities of serum SOD, LDH and CK, and taken hearts for measuring heart weight index (HWI), left ventricular mass index (LHWI), the contents of myocardial hydroxyproline (Hyp)and MDA, and observing the morphological changes of myocardial tissue by HE staining. RESULTS Compared with rats in normal group, rats in model group showed endurance value decrease, ECG abnormalities (arrhythmia and myocardial ischemia in waveform), increased HWI, LHWI (P<0.01), myocardial Hyp content, myocardial MDA level, and the level of serum LDH and CK, and reduced the serum SOD activity (P<0.05 or P<0.01). Compared with model group, CM could significantly increase endurance value, improve abnormal phenomenon of ECG, lower the HWI, LHWI, myocardial Hyp content, myocardial MDA level, and serum LDH and CK levels were lower, and serum SOD activity increased, especially in high dose group of CM (P<0.01). HE staining showed in the model group rat ventricular remodeling, myocardial rupture, a large number of collagen fibers, in the treatment group, ventricular remodeling and myocardial fibrosis were significantly improved. CONCLUSION Cinepazide maleate has protective effect on myocardial injury of rats induced by Iso.