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

被引:14
作者
Liu, Xuemei [1 ]
Tao, Ye [2 ]
Wang, Fengli [1 ]
Yao, Ting [3 ]
Fu, Chen [1 ]
Zheng, Hong [1 ]
Yan, Yan [1 ]
Liang, Xiao [1 ]
Jiang, Xiangning [4 ]
Zhang, Yunling [1 ]
机构
[1] Beijing Univ Chinese Med, Dongfang Hosp, Cent Lab, 6 Zone One Fangxingyuan, Beijing 100078, Peoples R China
[2] SIPO, Patent Examinat Coperat Ctr, Patent Off, Beijing 100190, Peoples R China
[3] China Japan Friendship Hosp, 2 YinghuaDongjie, Beijing 100029, Peoples R China
[4] Univ Calif San Francisco, Dept Pediat, 675 Nelson Rising Lane,Room 494, San Francisco, CA 94158 USA
来源
BMC COMPLEMENTARY AND ALTERNATIVE MEDICINE | 2017年 / 17卷
关键词
Cerebral ischemia; Myocardial injury; Oxidative stress; Mitochondria; Kudiezi injection; TILMICOSIN-INDUCED CARDIOTOXICITY; OXIDATIVE STRESS; ARTERY OCCLUSION; STROKE; ACID; CONSEQUENCES; MORTALITY; TOXICITY; MODELS;
D O I
10.1186/s12906-016-1514-1
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
Background: 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. Methods: 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. Results: 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. Conclusion: 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.
引用
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页数:10
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