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。
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 rag· 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 laetuside 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.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2012年第4期489-493,共5页
Chinese Journal of Pharmacology and Toxicology
基金
国家自然科学基金(81172953)
河南省教育厅自然科学研究基金(2009A310009)~~