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lactuside B降低脑缺血损伤大鼠海马和纹状体TRPM7 mRNA的表达
引用本文:詹合琴,贾岩龙,闫福林,牛秉轩,尹延彦.lactuside B降低脑缺血损伤大鼠海马和纹状体TRPM7 mRNA的表达[J].中国药理学与毒理学杂志,2012,26(4):489-493.
作者姓名:詹合琴  贾岩龙  闫福林  牛秉轩  尹延彦
作者单位:1. 新乡医学院药学院药理教研室,河南新乡,453003
2. 新乡医学院药学院药物化学教研室,河南新乡,453003
3. 新乡医学院药学院综合办公室,河南新乡,453003
基金项目:国家自然科学基金,河南省教育厅自然科学研究基金
摘    要:目的探讨lactuside B对大鼠脑缺血损伤后海马和纹状体TRPM7 mRNA表达的影响。方法采用大脑中动脉缺血再灌注损伤模型,SD雄性大鼠缺血2 h后再灌,分别于再灌后ip给予lactuside B 12.5,25和50 mg·kg-1,每天2次,每组1/2大鼠给药1 d,另1/2大鼠连续给药3 d,于末次给药后观察神经缺失症状并处死大鼠;RT-PCR技术检测大脑皮质和海马TRPM7 mRNA的表达。结果模型组大鼠各时间段神经缺失症状评分明显升高,海马和纹状体的TRPM7 mRNA表达均显著增加(P<0.01)。给予lactuside B12.5,25和50 mg·kg-11 d后,海马和纹状体TRPM7 mRNA表达分别为0.68±0.02,0.55±0.02和0.56±0.02,及0.32±0.02,0.25±0.01和0.35±0.01,与模型对照组比较均明显降低(P<0.01);给予lactuside B 12.5,25和50 mg·kg-1 3 d,海马和纹状体TRPM7 mRNA分别为0.29±0.02,0.18±0.01和0.26±0.01,及0.28±0.02,0.19±0.01和0.27±0.01,与模型对照组比较均明显降低(P<0.01)。结论lactuside B可降低海马和纹状体TRPM7基因的表达,提示该化合物对脑缺血损伤可能具有治疗作用。

关 键 词:lactuside  B  再灌注损伤    海马  纹状体  TRPM7阳离子通道
收稿时间:2011-11-16
修稿时间:2012-3-20

Inhibitory effect of lactuside B on TRPM7 mRNA expression in hippocampus and striatum in cerebral ischemic rats
ZHAN He-qin , JIA Yan-long , YAN Fu-lin , NIU Bing-xuan , YIN Yan-yan.Inhibitory effect of lactuside B on TRPM7 mRNA expression in hippocampus and striatum in cerebral ischemic rats[J].Chinese Journal of Pharmacology and Toxicology,2012,26(4):489-493.
Authors:ZHAN He-qin  JIA Yan-long  YAN Fu-lin  NIU Bing-xuan  YIN Yan-yan
Institution:1. Department of Pharmacology,School of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China;2. Department of Medicinal Chemistry,School of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China;3. General Office, School of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China
Abstract:OBJECTIVE To explore the effect of lactuside B on transient receptor potential melastatin 7(TRPM7) mRNA expression in rat hippocampus and striatum after cerebral ischemia injury. METHODS The middle cerebral artery occulsion was used to make the ischemia (2 h) reperfusion injury model. After reperfusion, the rats were respectively ip given lactuside B 12.5, 25 and 50 mg·kg-1 twice daily. Half of the rats of each group administered for 1 d while the rest administered continuously for 3 d. After the neurologic deficit score was observed in the last administration, the rats were sacrificed. The expression of TRPM7 mRNA on hippocampus and striatum was detected by RT-PCR. RESULTS Compared with sham group, the neurological lack symptom score in model group was significantly higher and the TRPM7 mRNA expression increased in hippocampus and striatum in rats. After lactuside B 12.5, 25 and 50 mg·kg-1 was administered for 1 d, TRPM7 mRNA expression was decreased in hippocampus and striatum (hippocampus: 0.68±0.02, 0.55±0.02 and 0.56±0.02; striatum: 0.32±0.02, 0.25±0.01 and 0.35±0.01). TRPM7 mRNA expression was lower after lactuside B administered for 3 d (hippocampus: 0.29±0.02, 0.18±0.01 and 0.26±0.01; striatum: 0.28±0.02, 0.19±0.01 and 0.27±0.01). CONCLUSION Lactuside B can reduce TRPM7 gene expression in hippocampus and striatum, suggesting that lactuside B play a positive therapeutic and protective role.
Keywords:lactuside B  reperfusion injury  brain  hippocampus  striatum  TRPM7 cation channel
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