Kudiezi injection mitigates myocardial injury induced by acute cerebral ischemia in rats.

Kudiezi injection mitigates myocardial injury induced by acute cerebral ischemia in rats.
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DOI:
10.1186/s12906-016-1514-1
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发表时间:
2017-01-05
影响因子:
--
通讯作者:
Zhang Y
Zhang Y
中科院分区:
医学3区
文献类型:
--
作者:
Liu X;Tao Y;Wang F;Yao T;Fu C;Zheng H;Yan Y;Liang X;Jiang X;Zhang Y

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苦碟子注射液是治疗脑梗塞、心绞痛的常用中药。本研究探讨了KDZ注射液对急性脑缺血所致心肌损伤的治疗作用及其可能的保护机制。将大鼠分为假手术组、缺血6 h组和KDZ治疗组(KDZ)。神经功能缺损由Garcia评分确定。采用氯化三苯基四氮唑(TTC)染色法测量脑梗死体积,并测定脑含水量。测定血清肌酸激酶(CK)、乳酸脱氢酶(LDH)、肌酸激酶-心肌带(CK-MB)活性、心肌组织丙二醛(MDA)、谷胱甘肽(GSH)含量、超氧化物歧化酶(SOD)活性和线粒体细胞色素c氧化酶(考克斯)活性。RT-PCR检测心肌组织线粒体考克斯I、考克斯III mRNA的表达。缺血6 h组大鼠神经功能受损,脑水肿明显。TTC染色显示缺血6 h组梗死面积较假手术组大。与假手术组比较,缺血6 h组心肌缺血性改变(心肌细胞间隙增宽、裂纹、明显水肿),血清CK-MB活性、CK和LDH水平升高。与假手术组相比,缺血6 h组心电图中高频(HF)和中频(MF)明显降低。缺血6 h心肌组织中考克斯酶活性较假手术组升高,而SOD、GSH、MDA水平及考克斯I、考克斯III mRNA表达无明显变化。注射KDZ可减少神经功能缺损、脑水肿、细胞间隙和梗死面积。与缺血6 h组相比,能降低血清CK-MB活性,降低心肌组织中CK、LDH水平及MDA水平。与假手术组相比,KDZ可显著增加心肌组织GSH水平、SOD活性、线粒体考克斯活性及考克斯I、考克斯III mRNA表达。KDZ注射液对大鼠脑缺血有保护作用。KDZ注射液还能减轻急性脑缺血后大鼠心肌损伤。其机制可能与脑缺血后氧化应激/抗氧化能力的调节有关。
Kudiezi (KDZ) injection is commonly used in traditional Chinese medicine as treatment for cerebral infarction and angina pectoris. The present study investigated the therapeutic effects of KDZ injection on myocardial injury induced by acute cerebral ischemia and the possibly protective mechanisms. Rats were divided into three groups: sham, 6h-ischemia, and KDZ treatment (KDZ). The neurological deficits were determined by the Garcia score. The cerebral infarct volume was measured by 2,3,5-triphenyltetrazolium chloride (TTC) staining, and brain water content was also evaluated. Serum creatinine kinase (CK), lactate dehydrogenase (LDH), and creatine kinase-myocardial band (CK-MB) activity, myocardial tissue malondialdehyde (MDA) levels, L-Glutathione (GSH) levels, and superoxide dismutase (SOD) activity as well as mitochondrial cytochrome c oxidase (COX) activity were determined. Mitochondrial COX I and COX III mRNA expressions of myocardial tissues were measured by RT-PCR. Impaired neurological function and brain edema were observed in the 6h-ischemia group. TTC staining showed that the 6h-ischemia group had larger infarct zones than the sham group. Myocardial ischemic changes (widened myocardial cell gap, cracks, and obvious edema) were detected in the 6h-ischemia group compared with the sham group, with elevated serum CK-MB activity and CK and LDH levels. Electrocardiography showed lower medium frequency (MF) and high frequency (HF) in the 6h-ischemia group compared with the sham group. In myocardial tissue, COX activity was elevated in the 6h-ischemia compared with the sham group, while SOD, GSH, and MDA levels, and COX I and COX III mRNA expressions remained unchanged. KDZ injection decreased neurological impairment, brain edema, gaps between cells, and infarct size. Compared with the 6h-ischemia group, it reduced serum CK-MB activity and CK and LDH levels, and MDA levels in myocardial tissue. KDZ significantly increased GSH levels, SOD activity, and mitochondria COX activity and the expression of COX I and COX III mRNA in myocardial tissue compared with the sham group. KDZ injection had a protective effect against cerebral ischemia in rats. KDZ injection could also alleviate myocardial injury after acute cerebral ischemia in rats. The possible mechanisms involve the regulation of the oxidative stress/antioxidant capacity after cerebral ischemia.
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