茶多酚对异丙肾上腺素致大鼠心肌肥厚的保护作用

目的观察茶多酚对大鼠心肌肥厚的保护作用并讨论其相关可能作用机制。方法采用皮下注射异丙肾上腺素（ISO）建立大鼠心肌肥厚模型,将28只SD大鼠随机分为对照组、模型组、美托洛尔组、茶多酚组,灌胃给药连续14d后,取心脏称重后计算全心重量指数及左心重量参数;分别检测测定心肌组织一氧化氮合酶（NOS）活性及心肌组织血管紧张素Ⅱ（AngⅡ）及钙调神经磷酸酶（CaN）的水平。结果与模型组相比,茶多酚能显著改善心脏质量指数,心肌组织NOS活性显著升高、AngⅡ含量降低、CaN活性明显降低。结论茶多酚对异丙肾上腺素所致大鼠心肌肥厚具有保护作用,其作用机制可能与提高NO水平、降低CaN活性、抑制AngⅡ有关。     

心肌自噬在异丙肾上腺素诱导心肌肥厚中的作用

目的 探讨心肌自噬在异丙肾上腺素（ISO）诱导大鼠心肌肥厚中的作用。方法 将 29只大鼠随机分为 3组：皮下联合腹腔注射生理盐水（Con）组 9只、腹腔注射生理盐水联合皮下注射异丙肾上腺（ISO）组 10只、腹腔注射雷帕霉素（RAP）联合皮下注射 ISO（ISO+RAP）组 10 只。连续干预 14 d 后,将 Con 组和 ISO 组存活大鼠（Con,n=9;ISO,n=8）行心脏超声检查左室壁厚度及左室射血分数（LVEF）,再将各组大鼠腹腔注射过量的 10%水合氯醛处死,摘除心脏,计算心脏体质量指数（HWI）。心肌组织病理切片行 HE染色和 Masson染色,Western blot检测 p62表达和LC3Ⅱ/Ⅰ比值,透射电镜观察心肌组织自噬泡数量。结果 与 Con组比较,ISO组左室壁厚度和 LVEF明显增加（P＜0.01）。与 Con组比较,ISO组和 ISO+RAP组的 HWI增大（P＜0.01）,且 ISO+RAP组的 HWI小于 ISO组（P＜0.01）。与Con组比较,ISO组心肌病理切片显示心肌组织病理性肥厚改变明显;而与 ISO组比较,ISO+RAP组心肌组织病理性肥厚明显改善。与 Con 组比较,ISO 组心肌组织 LC3Ⅱ/Ⅰ比值下调,而 p62 表达上调,自噬泡数量明显减少（P＜0.05）;与 ISO组比较,ISO+RAP组心肌组织 LC3Ⅱ/Ⅰ比值上调,而 p62表达下调,自噬泡数量明显增多（P＜0.01）。结论 上调心肌自噬活性可以逆转 ISO诱导的病理性心肌肥厚。     

cTnI、AST及CK在鉴别诊断大鼠骨骼肌与心肌损伤应用价值的比较

目的探讨心肌肌钙蛋白Ⅰ(cardiac troponin Ⅰ,cTnI)在鉴别诊断大鼠骨骼肌与心肌损伤应用价值。方法 32只SD大鼠随机分为4组:心肌损伤组,单次背部皮下注射异丙肾上腺素;骨骼肌损伤组,单次单侧胫骨肌注射布比卡因;联合损伤组,单次单侧胫骨肌注射布比卡因及背部皮下异丙肾上腺素;正常对照组,不给予任何药物。予给药后24h,检测血清AST,CK及cTnI,常规HE染色观察骨骼肌和心肌受损情况。结果心肌损伤组和联合损伤组血清cTnI均显著高于正常对照组和骨骼肌损伤组(P<0.01),而联合损伤组和心肌损伤组AST与骨骼肌损伤组无明显差异(P>0.05),心肌损伤组CK与骨骼肌损伤组无明显差异(P>0.05)。结论cTnI在鉴别大鼠心肌及骨骼肌损伤上较AST、CK有较高的敏感性,并且在一定程度上能够降低误诊及漏诊率。     

黄芪甲苷激活ROCK/JNK介导自噬减轻异丙肾上腺素诱导的小鼠心肌纤维化

目的 探讨黄芪甲苷（AS-Ⅳ）激活ROCK/JNK调控自噬,改善异丙肾上腺素（ISO）诱导的小鼠心肌纤维化(MF)的作用及机制。方法 将小鼠随机分为对照组、ISO诱导心肌纤维化组（MF组）、黄芪甲苷组、黄芪甲苷与Y-33075（ROCK抑制剂）联合组（黄芪甲苷+Y-33075组）,重复给药持续30 d后,检测小鼠血清LDH、BNP、CTGF水平,超声检测心功能指标,天狼猩红、Masson染色检测各组小鼠心肌结构及组织纤维化程度, DHE检测各组小鼠心肌组织氧化应激（ROS）水平,蛋白印迹法检测心肌组织ROCK、JNK、Atg5、Beclin 1、LC3 Ⅰ/Ⅱ表达。结果 与黄芪甲苷组比较,黄芪甲苷+Y-33075组的EF值降低,心肌纤维化程度增加,血清LDH、BNP、CTGF水平升高,心肌组织ROS水平增高,ROCK、JNK、Atg5、Beclin 1、LC3 Ⅰ/Ⅱ表达水平表达降低（P<0.05）,表明Y-33075能够阻断黄芪甲苷对心肌纤维化的保护作用,并抑制黄芪甲苷对ROCK和JNK的调控。结论 黄芪甲苷通过激活ROCK/JNK信号促进自噬减轻小鼠心肌纤维化。     

黄柏提取物对大鼠心肌损伤的保护作用

摘 要 目的：探讨黄柏水提物和醇提物对垂体后叶素和盐酸异丙肾上腺素致大鼠心肌损伤的保护作用及其可能的作用机制。方法: 将SD大鼠随机分为正常对照组、模型组、复方丹参片组、黄柏水提组、黄柏醇提组,建立垂体后叶素和盐酸异丙肾上腺素大鼠心肌损伤模型,检测血清中肌酸激酶（CK）、乳酸脱氢酶（LDH） 活性、心肌组织超氧化物歧化酶（SOD）活性和丙二醛（MDA）含量。 结果: 与正常对照组比较,垂体后叶素建立的大鼠心肌损伤模型组血清LDH活性、CK活性和心肌组织MDA含量明显升高,心肌组织SOD活性明显降低（P<0.01）;盐酸异丙肾上腺素建立的大鼠心肌损伤模型组心肌组织MDA含量明显升高,心肌组织SOD活性明显降低（P<0.01）。与垂体后叶素建立的大鼠心肌损伤模型组相比较,各给药组血清LDH活性、CK活性和心肌组织MDA含量明显降低,心肌组织SOD活性明显升高,差异有统计学意义（P<0.05或P<0.01）;与盐酸异丙肾上腺素建立的大鼠心肌损伤模型组相比较,各给药组心肌组织中MDA含量明显降低,SOD活性明显升高,差异有统计学意义（P<0.05或P<0.01）。结论:黄柏提取液对垂体后叶素和盐酸异丙肾上腺素引起的大鼠心肌损伤有一定保护作用。     

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。     

糖心通对心肌缺血大鼠心肌酶及炎性因子的影响

目的：观察糖心通对异丙肾上腺素（ISO）所致心肌缺血模型大鼠心肌酶及相关炎性因子的影响。方法：皮下注射ISO复制心肌缺血模型,观察糖心通对该模型大鼠血清肌酸激酶（CK）、乳酸脱氢酶（LDH）、肿瘤坏死因子（TNF）、白介素石（IL-6）的影响。结果：糖心通能拮抗心肌缺血损伤引起的CK、LDH的升高,并抑制炎性因子TNF—α、IL-6水平的升高。结论：糖心通对ISO所致心肌缺血模型大鼠心肌有较好的保护作用。     

异丙肾上腺素和精氨酸血管加压素诱导的大鼠心肌损伤模型比较

目的 分别建立异丙肾上腺素（ISO）和精氨酸血管加压素（AVP）诱导的大鼠心肌损伤模型,并将两种模型进行比较。方法 分别建立雄性SD大鼠AVP、ISO心肌损伤模型,ISO模型组大鼠按30 mg/kg的剂量以多点sc方式给药,连续2 d,1次/d;AVP模型组大鼠尾iv精氨酸血管加压素0.05 mg/kg。超声测量心功能,监测大鼠心电图,测量大鼠血清中心钠素（ANP）、脑利钠肽（BNP）、乳酸脱氢酶（LDH）、肌酸激酶（CK）、天冬氨酸转氨酶（AST）、超氧化物歧化酶（SOD）的水平,并对大鼠心脏进行HE染色,观察切片。结果 AVP模型组大鼠心电图ST段较对照组显著上升（P<0.05）,ISO模型组大鼠心电图紊乱且短期内不能恢复。超声结果显示,与对照组比较,ISO和AVP模型组大鼠的左心室舒张末期内径（LVDd）和左心室收缩末期内径（LVDs）显著增加（P<0.05）,射血分数（EF）显著下降（P<0.05）,E/A下降至1以下。AVP和ISO模型组大鼠ANP水平均显著高于对照组（P<0.01）;ISO模型组大鼠BNP水平显著高于对照组（P<0.01）。AVP和ISO模型组大鼠CK、LDH、AST水平均显著高于对照组（P<0.05）,ISO模型组大鼠CK、LDH水平均显著高于AVP模型组（P<0.05）;ISO模型组大鼠SOD含量显著低于对照组（P<0.05）。HE染色结果显示,对照组心肌细胞结构清晰排列紧密,AVP模型组心肌细胞出现细胞核溶解和空泡变性,ISO模型组出现心肌组织纤维化和炎细胞浸润。结论 ISO和AVP诱导的大鼠心肌损伤模型均有明显的心脏病理性改变,且前者对大鼠心肌的损伤的程度较大,初步判断可能是由于缺氧时间更长造成的。     

复方丹参滴丸对心肌保护作用的实验研究

为探讨复方丹参滴丸（DSP）对心肌损伤的保护作用机制，将120只大鼠随机分为4组：异丙肾上腺素（ISO）损伤组、DSP保护组、DSP＋ISO组及正常对照组。应用ISO腹腔内注射造成心肌缺血损伤，测定大鼠血清及心肌组织中脂质过氧化物丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性及血浆中内皮素（ET）和血清中一氧化氮（NO）含量的变化。结果表明，DSP保护组血浆中NO含量升高，与正常对照组差异有显性；DSP保护组注射ISO后MDA、SOD、ET及NO变化程度明显小于单纯ISO组，差异有显性。结论：复方丹参滴丸具有良好的抗急性心肌缺血损伤作用，其作用机制与抗自由基及血管内皮保护效应密切相关。     

理气活血滴丸含药血清对ISO诱导乳鼠心脏成纤维细胞转分化的影响及其机制研究

目的：研究理气活血滴丸含药血清对异丙肾上腺素（isoprenaline,ISO）诱导的乳鼠心脏成纤维细胞（CFs）转分化的影响及其机制。方法：离体培养SD乳鼠CFs并经CCK-8法筛选理气活血滴丸含药血清的最适工作浓度。将细胞分为正常对照组（NC组）、空白大鼠血清组（BRS组）、ISO诱导模型组（NC+ISO组）、空白大鼠血清+ISO诱导模型组（BRS+ISO组）、理气活血滴丸含药血清+ISO诱导模型组（LQHXDP+ISO组）。生化法和ELISA法分别检测羟脯氨酸（Hyp）和TGF-β1水平,流式细胞术和Western blot分别检测细胞周期分布和CollagenⅠ、CollagenⅢ、α-SMA、IL-6、p-STAT3、STAT3蛋白表达情况。结果：经Vimentin免疫荧光鉴定所得细胞为CFs,10%的理气活血滴丸以175.0 mg·kg–1剂量灌胃大鼠制备的含药血清为最佳工作浓度;与NC和BRS组相比,经ISO诱导的CFs增殖活力显著增加,细胞培养上清液中Hyp、TGF-β1含量显著增加,S期细胞显著增多,CollagenⅠ、CollagenⅢ、α-SMA、IL-6、p-S...     

Enhancement of hydralazine hypotension by low doses of isoniazid. Possible role of semicarbazide-sensitive amine oxidase inhibition

The influence of pretreatment with 1 through 300 mg/kg ip of isoniazid (ISO) on blood pressure and heart rate responses to 0.1 mg/kg iv of hydralazine (HYD) was assessed in rats anesthetized with chloralose--urethane. HYD hypotension was significantly enhanced by ISO at doses between 3 and 300 mg/kg ip. Heart rate was not influenced by HYD in control or pretreated animals. Depressor responses to 0.2 mg/kg iv of pinacidil (PIN) were also potentiated by ISO at 100 and 300, but not at 30 mg/kg. Similarly, ISO decreased cerebral gamma-aminobutyric acid (GABA) at the two highest doses; 30 mg/kg was without effect. Pretreatment of rats with ISO at 1 through 300 mg/kg failed to influence HYD-induced relaxation of aortic rings. These results were interpreted as indicating that potentiation of HYD hypotension by high doses of ISO is not specific for that vasodilator and is related to decreased cerebral GABA, as postulated previously. Lower doses could specifically potentiate the HYD-induced hypotensive effect by inhibition of semicarbazide-sensitive amine oxidase (SSAO), since both ISO and HYD are potent inhibitors of this enzyme. In support of this hypothesis, the SSAO inhibitors, benserazide (100 mg/kg ip) and mexiletine (50 mg/kg ip), were also found to enhance HYD hypotension.     

黄芩苷对心力衰竭大鼠心律失常及心室肌细胞内质网应激-肌电稳定性的影响

目的　探究黄芩苷对心力衰竭大鼠室性心律失常及心室肌细胞内质网应激-肌电稳定性的影响。方法　雄性6周龄Wistar大鼠72只,随机分为对照组,模型组,美托洛尔组,黄芩苷低、中、高剂量组,每组12只。模型组给予异丙肾上腺素（ISO）后颈部皮下注射5 mg/（kg·d）,对照组给予等体积0.9%NaCl注射液后颈部皮下注射,连续注射7 d;美托洛尔组及黄芩苷低、中、高剂量组在模型组基础上分别给予美托洛尔10 mg/（kg·d）及25、50、100 mg/（kg·d）黄芩苷灌胃,对照组给予药物等体积0.9%NaCl注射液灌胃,连续给药4周。于4周末行心电图及多普勒超声检测各组大鼠心率、室性早搏发生情况及测定左心室射血分数（LVEF）、左心室舒张末期内径（LVEDd）、左心室收缩末期内径（LVESd）;酶联免疫吸附测定（ELISA）法检测各组大鼠血清人基质裂解素2（ST2）、脑钠肽（BNP）含量。每组取6只大鼠制备Langendorff离体心脏灌注模型,记录和测量心肌单相动作电位复极90%的时程（MAPD90）、心室肌细胞有效不应期（ERP）及ERP/MAPD90比值;另外6只大鼠行心室肌TUNEL染色后检测其心肌细胞凋亡情况;Western blot检测各组大鼠心室肌细胞葡萄糖调节蛋白78（GRP78）、肌醇需酶1（IRE1）、C/EBP环磷酸腺苷反应元件结合转录因子同源蛋白（CHOP）及缝隙连接蛋白43（Cx43）蛋白表达。结果　与对照组比较,模型组大鼠心率增快,易发生室性早搏,LVESd、LVEDd升高,LVEF降低,血清ST2、BNP含量升高,心室肌细胞ERP/MAPD90降低,凋亡指数（AI）升高,GRP78、IRE1、CHOP表达升高,Cx43表达降低（均P＜0.05）;与模型组比较,黄芩苷低、中、高剂量组上述指标均明显改善,且呈剂量依赖性（P＜0.05）。结论　黄芩苷具有改善ISO所致心力衰竭大鼠室性心律失常及心功能的作用,其机制可能与抑制心室肌细胞内质网应激及细胞凋亡、提高肌电稳定性相关。     

高频超声心动图评价异丙肾上腺素造模大鼠心脏结构及心功能改变的实验研究

目的应用高频超声心动图动态观察异丙肾上腺素(isoproterenol,ISO)造模大鼠心脏结构和心功能的改变,探讨该方法的可行性、准确性及影响因素,评价造模大鼠左室肥厚和心力衰竭时的心功能影响与机制。方法20只Wistar大鼠随机分成对照组、ISO组。通过大剂量注射ISO制成心肌肥厚-心力衰竭模型。对2组大鼠行经胸超声心动图监测。结果高频超声可以清晰显示大鼠心脏结构。超声测定的ISO组与对照组在室壁厚度、心脏结构及心功能变化差异有统计学意义(P<0.05)。超声测得大鼠心脏质量与尸检测得结果高度相关(r=0.82)。结论高频超声心动图是可以准确评价造模大鼠的心脏结构及心功能变化的无创方法;大剂量ISO可复制心肌肥厚、心力衰竭的动物模型。     

Effects of Lagenaria sicessaria fruit juice on lipid profile and glycoprotein contents in cardiotoxicity induced by isoproterenol in rats

This study investigated antihyperlipidemic effects of Lagenaria siceraria fruit juice (LSFJ) in isoproterenol (ISO)induced cardiotoxicity in rats. Rats treated with ISO (200 mg/kg, s.c.) showed a significant increase in the levels of triglycerides, cholesterol, and free fatty acids, in both serum and heart tissue. An increase in the levels of phospholipids, low-density lipoprotein, and very low-density lipoprotein-cholesterol, and decrease in high-density lipoprotein-cholesterol in serum and phospholipid levels in the heart were observed. ISO intoxicated rats also showed a significant decrease in the activities of lecithin: cholesterol acyl transferase, whereas lipoprotein lipase was found to be increased. Administration of LSFJ (400 mg/kg, p.o.) for 30 consecutive days and challenged with ISO on day 29th and 30th significantly attenuated these alterations and restored the levels of serum and heart lipids along with lipid metabolizing enzymes. Histopathological observations were also in correlation with the biochemical parameters. These findings indicate the protective effect of LSFJ during ISO-induced cardiotoxicity in rats.     

Fixed combination isosorbide dinitrate-hydralazine for nitric-oxide-enhancing therapy in heart failure

The major advances in our understanding and management of heart failure (HF) in recent decades have not fully benefited all segments of our population. HF still represents a growing epidemic, especially for African-Americans, in whom the burden of HF is even greater. The recently reported beneficial effects of the fixed combination of isosorbide dinitrate and hydralazine (ISDN+HYD) in the African-American Heart Failure Trial (A-HeFT), has led to both the FDA approval of this agent and its endorsement by the latest HF guidelines. The properties of ISDN+HYD are well known as its components are mature agents, readily available in generic formulations that have been used for decades in other indications. However, fixed-dose ISDN+HYD represents the first drug to undergo targeted clinical development and to be approved for use in a specific ethnic group. As such, A-HeFT and the approval of ISDN+HYD represent landmark events that merit further scrutiny.     

Efficacy of grape seed proanthocyanidins on serum and heart tissue lipids in rats subjected to isoproterenol-induced myocardial injury

The present study was aimed to evaluate the preventive role of grape seed proanthocyanidins (GSPs) on serum and tissue lipid enzymes in isoproterenol (ISO)-induced myocardial injury in male Wistar albino rats. GSP was administered orally to rats (150-180 g) in three different doses, by gastric gavage (50, 100 and 150 mg/kg GSP), 6 days a week for 5 weeks. At the end of this period, all the rats, except the normal untreated rats that served as the control group, were administered ISO, 85 mg/kg subcutaneously, for 2 consecutive days to induce myocardial injury. After 48 h, rats (n=6 per group) were anesthetized with anesthetic ether, sacrificed and the levels of biochemical observations of the serum and heart tissues were performed. Biochemical assessment of myocardial injury was done by measuring the activities of serum thiobarbituric acid reactive substances and plasma lactate, which were significantly elevated in the rats administered with ISO. Further, our results suggest that prior administration of GSPs significantly maintained the cholesterol, phospholipids, triglycerides, and free fatty acids levels in serum and heart tissue of the ISO-induced myocardial injury in rats. The experiments conclude that GSPs possess cardioprotective and hypolipidemic effect on the treatment of ISO-induced myocardial injury.     

辛伐他汀对慢性心力衰竭患者功能变化及CRP、BNP水平的影响

目的观察他汀类药物短期应用对慢性心力衰竭患者心功能、细胞因子(C反应蛋白、脑利尿钠肽)水平的影响。方法将106例慢性心力衰竭患者(NYHA分级Ⅱ～Ⅲ级)随机分为两组,治疗组(54例)和对照组(52例),两组都给予β受体阻滞剂、ACEI、利尿剂及地高辛治疗,治疗组再给予辛伐他汀40mg,每晚一次,共服6个月,治疗前后检查心脏彩超,评价心功能,测定C反应蛋白、脑利尿钠肽及血脂水平。结果 6个月后治疗组低密度脂蛋白、胆固醇水平明显降低,心功能有明显改善(P<0.01),左室射血分数有明显提高(P<0.01),C反应蛋白、脑利尿钠肽有明显的降低(P<0.01),而对照组前后无明显改变。结论辛伐他汀能降低血浆细胞因子(C反应蛋白、脑利尿钠肽)水平,改善心功能,有利于慢性心力衰竭的治疗。     

黄芪甲苷对异丙肾上腺素诱导大鼠 心肌肥厚的保护作用研究

摘要：目的 探讨黄芪甲苷对异丙肾上腺素（ISO）诱导的大鼠心肌肥厚的保护作用机制。方法 健康SPF级SD 大鼠24只,随机分为4组,对照组（与ISO组等体积的生理盐水腹腔注射,之后与黄芪甲苷组等体积生理盐水灌胃）、 ISO组［ISO 3 mg/ （kg·d）腹腔注射,与黄芪甲苷等体积生理盐水灌胃］、黄芪甲苷组［与ISO等体积生理盐水腹腔注射, 黄芪甲苷溶液5 mg/ （kg·d）灌胃］、黄芪甲苷+ISO组［ISO 3 mg/ （kg·d）腹腔注射,黄芪甲苷溶液5 mg/ （kg·d）灌胃］,每 组6只,共处理14 d。处理结束后取大鼠左心室,计算左心室质量指数（左心室质量/体质量）。HE染色观察左心室心 肌肥厚情况,比较心肌横截面积的差异。以二氯荧光素（DCF）为探针检测心肌线粒体活性氧（ROS）生成速率; Western blot 法检测大鼠心肌NADPH氧化酶4（NOX4）和心房利钠肽（ANP）蛋白表达水平;RT-qPCR检测大鼠心肌 ANP在转录水平的表达情况。结果 与对照组相比,ISO组左心室质量指数明显升高,心肌横截面积扩大,心肌线粒 体ROS生成速率加快,NOX4蛋白、ANP mRNA及蛋白表达水平均明显升高（P < 0.05）。而ISO+黄芪甲苷组与ISO组 相比,上述指标均明显改善,主要表现为心肌横截面积缩小,ROS生成速率减慢,NOX4蛋白、ANP mRNA及蛋白表达 明显下降,差异均有统计学意义（P＜0.05）。结论 黄芪甲苷对ISO诱导的大鼠心肌肥厚具有确切的保护作用,且该 保护作用可能与黄芪甲苷降低氧化应激反应相关。     

氯沙坦对自发性高血压大鼠细胞外信号调节激酶活性和B型利钠肽表达的影响

目的　探讨氯沙坦治疗高血压心肌肥厚的作用机制。方法　选择同周龄WistarKyoto(WKY)大鼠作正常对照,将2 1只14周龄雄性自发性高血压大鼠(SHR)随机分成3组:模型组、肼屈嗪组(10mg·kg- 1·d- 1)和氯沙坦组(10mg·kg- 1·d- 1)。用West ern印迹方法检测大鼠心肌总细胞外信号调节激酶(t ERK)、磷酸化ERK(p ERK)及有丝分裂素激活蛋白激酶磷酸酶 1(MKP 1)水平;用RT PCR法半定量测定大鼠心肌中B型利钠肽(BNP)mRNA的含量;酶联免疫吸附法检测大鼠血浆BNP水平。结果喂药10周后,氯沙坦组和肼屈嗪组血压相似,均显著低于模型组(n =7,P <0 .0 1)。氯沙坦组心肌肥厚指数显著低于肼屈嗪组和模型组(n =7,P <0 .0 1) ,与WKY组无差异(n =7,P >0 .0 5 ) ;肼屈嗪组和模型组心肌肥厚指数无差异(n =7,P >0 .0 5 )。4组大鼠t ERK水平无显著性差异(n =7,P >0 .0 5 ) ;氯沙坦组心肌p ERK ,p ERK/t ERK及MKP 1水平均显著低于SHR肼屈嗪组和SHR模型组(n =7,P <0 .0 5 ) ,与WKY组无差异(n =7,P >0 .0 5 )。肼屈嗪组和模型组心肌p ERK ,p ERK/t ERK及MKP 1水平无差异(n =7,P >0 .0 5 )。氯沙坦组大鼠心肌BNPmRNA和血浆BNP水平显著低于SHR肼屈嗪组和模型组(n =7,P <0 .0 5 ) ,与WKY组无差异(n =7,P >0 .0 5 ) ;肼屈嗪组和SHR模型组大鼠     

Cardioprotective effects of cerebrolysin on the lesion severity and inflammatory factors in a rat model of isoproterenol-induced myocardial injury

BackgroundMyocardial injury (MI) is an important heart condition and a major cause of morbidity and mortality worldwide. The current study was designed to investigate the cardioprotective effects of cerebrolysin (CLY) on the lesion severity and inflammatory factors in male rats using isoproterenol (ISO)-induced MI model.MethodsMI in rats was induced by injecting ISO (100 mg/kg) subcutaneously (sc) on the first 2 days. Then, CLY (5 ml/kg) was injected intraperitoneally (ip) post-treatment for 7 days. On the 3rd day, creatine phosphokinase (CK-MB) and cardiac troponin I (cTnI) levels in serum and, on the 10th day, the TNF-α and IL6 levels in serum and heart tissue were measured by enzyme-linked immunosorbent assay (ELISA). Finally, the heart of each rat was dissected out and stained for histopathological examination.ResultsOn the 3rd day, the serum CK-MB and cTnI levels in the ISO and CLY + ISO groups were significantly increased compared with that in the control and CLY + Sal groups. One week after the induction of MI, ISO administration showed a significant increase in the serum level of TNF-α in the ISO group compared with that in the control and CLY + Sal groups. Also, our findings showed only a moderate reduction in inflammatory cell infiltration and extent of edema following CLY treatment in the CLY + ISO group. Also, CLY induced vascular proliferation in the heart tissue.ConclusionsWe conclude that the severity of pathological changes induced by ISO in MI (e.g. inflammation and edema) can be limited by CLY treatment.