Protective effect of Sheng-Nao-Kang decoction on focal cerebral ischemia-reperfusion injury in rats

被引:38
作者
Chen, Lin [1 ]
Zhao, Ye [1 ]
Zhang, Tianlong [2 ]
Dang, Xuan [1 ]
Xie, Renming [1 ]
Li, Zhenzhi [1 ]
Li, Yang [1 ]
Li, Yuli [1 ]
Zhao, Wenna [1 ]
Song, Hongru [3 ]
机构
[1] Northwest Univ, Biomed Key Lab Shaanxi Prov, Xian 710069, Peoples R China
[2] Northwest Univ, Coll Life Sci, Xian 710069, Peoples R China
[3] 323rd Hosp Peoples Liberat Army, Xian 710069, Peoples R China
关键词
Sheng-Nao-Kang decoction; Focal cerebral ischemia-reperfusion injury; Anti-oxidation; Anti-apoptosis; iNOS; ISCHEMIA/REPERFUSION INJURY; ARTERY OCCLUSION; OXIDATIVE STRESS; BRAIN; CASPASE-3; APOPTOSIS; INFLAMMATION; EXPRESSIONS; INHIBITION; ACTIVATION;
D O I
10.1016/j.jep.2013.10.015
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ethnopharmacological relevance: Sheng-Nao-Kang decoction (SNK), a modified traditional Chinese medicine (TCM), has been used clinically for the treatment of acute and chronic cerebrovascular related diseases. To evaluate the protective effect of SNK on focal cerebral ischemia-reperfusion (I/R) injury in rats and investigate the underlying mechanisms. Materials and methods: Focal cerebral I/R injury in rats was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion for 24 h. Adult male Sprague-Dawley (SD) rats were randomly divided into six kinds of groups: Sham group; I/R group; SNK-treated groups at doses of 0.7 g/kg, 1.4 g/kg and 2.8 g/kg; and nimodipine (NMP)-treated group. The recoveries of neurological function in rats were estimated by neurological defect scoring and 2,3,5-triphenyltetrazolium chloride (TTC) staining after 24 h reperfusion. Various biochemical indexes in serum were assayed by colorimetry, including malondialdehyde (MDA), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), inducible nitric oxide synthase (iNOS) and total nitric oxide synthase (TNOS). Histological structures of the brain in rats were observed by hematoxylin and eosin (H&E) staining. Immunohistochemistry was performed to detect the caspase-3 protein content in rats. Results: SNK administration significantly reduced the neurological defect scores and lessened the cerebral infarction volume. The treatment of SNK lowered MDA content, up-regulated SOD and GSH-Px levels, down-regulated iNOS and TNOS levels in serum. Furthermore, histological examination indicated that dense neuropil and largely surviving neurons were seen in SNK-treated rats. SNK administration restrained the expression of caspase-3 positive protein significantly. Conclusion: The results suggest that SNK demonstrates a strong and ameliorative effect on cerebral I/R damage in rats. The protective mechanisms of SNK are associated with its properties of anti-apoptosis and anti-oxidation as well as regulation of iNOS and TNOS. (C) 2013 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:228 / 236
页数:9
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