首页> 中文期刊> 《中国中西医结合急救杂志》 >人参皂苷Rb1预处理对急性束缚性应激大鼠海马组织脑源性神经营养因子表达的影响

人参皂苷Rb1预处理对急性束缚性应激大鼠海马组织脑源性神经营养因子表达的影响

             

摘要

目的 观察人参皂苷Rb1预处理对急性束缚性应激大鼠海马组织脑源性神经营养因子(BDNF)表达的影响.方法 将18只SD大鼠按随机区组法分成正常对照组、急性束缚应激模型组、人参皂苷Rb1组,每组6只.模型制备采用专业大鼠固定器束缚2h模拟急性束缚性应激状态;人参皂苷Rb1组于制模前30 min腹腔注射人参皂苷Rb1 40 mg/kg,正常对照组不进行任处理.用酶联免疫吸附试验(ELISA)测定制模前后大鼠血浆皮质酮(CORT)和促肾上腺皮质激素(ACTH)的水平.采用实时荧光定量反转录-聚合酶链反应(RT-PCR)检测大鼠海马组织中BDNF mRNA的表达水平,用蛋白质免疫印迹试验(Western Bolt)检测大鼠海马组织的BDNF蛋白表达水平.结果 急性束缚应激模型组制模后血浆CORT和ACTH含量较制模前明显升高[CORT(μg/L):3.79±0.50比2.06±0.35),ACTH(μg/L):1.69±0.12比0.94±0.12],差异均有统计学意义(均P< 0.05).与正常对照组比较,急性束缚应激模型组海马组织BDNF的mRNA和蛋白表达水平水平均明显降低[BDNFmRNA(A值):42.87±5.56比109.39±9.11,BDNF蛋白(灰度值):0.94±0.02比1.02±0.03,均P<0.01];与急性束缚应激模型组比较,人参皂苷Rb1组海马组织BDNF的mRNA(113.73±6.24比42.87±5.56)和蛋白(1.04±0.02比0.94±0.02)表达水平均明显升高(均P<0.05).结论 人参皂苷Rbl预处理可以维持急性束缚性应激大鼠模型海马组织BDNF的mRNA和蛋白表达水平,从而缓解急性束缚性应激所导致的损害.%Objective To investigate the effects of ginsenoside Rb1 pretreatment on the expression of brain derived neurotrophic factor (BDNF) in hippocampus of rat models under acute immobilization stress.Methods Eighteen Sprague-Dawley (SD) rats were randomly divided into three groups (each n =6):normal control group,acute immobilization stress model group,and ginsenoside Rbl group.The rats in acute immobilization stress model group and ginsenoside Rb1 group were exposed to acute immobilization for 2 hours.Thirty minutes before the modeling,ginsnoside Rb1 (40 mg/kg) was injected intraperitoneally into rats in the ginsenoside Rbl group,and the control group was not treated.The enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of plasma cortisol (CORT) and adrenocorticotropic hormone (ACTH).The real-time fluorescence quantitative reverse transcription-polymerase chain reaction (RT-PCR) was applied to examine the expression of BDNF mRNA in rat hippocampus and its expression of BDNF protein was measured by Western Blot.Results In acute immobilization stress model group,compared with those before modeling,the plasma CORT and ACTH concentrations were significantly higher after modeling [CORT (μg/L):3.79 ± 0.50 vs.2.06 ± 0.35,ACTH (μg/L):1.69 ± 0.12 vs.0.94 ± 0.12,both P <0.05];compared with the normal control group,the mRNA and protein expressions of BDNF in hippocampus in the acute immobilization stress model group were decreased significantly [BDNF mRNA (A value):42.87 ± 5.56 vs.109.39 ± 9.11,BDNF protein (grey value):0.94 ± 0.02 vs.1.02 ± 0.03,both P < 0.01];compared with acute immobilization stress model group,the mRNA (113.73 ± 6.24 vs.42.87 ± 5.56) and protein expressions (1.04 ± 0.02 vs.0.94 ± 0.02) of BDNF in hippocampus of pre-treatment groups were significantly higher (all P < 0.05).Conclusions The results suggest that pretreatment with ginsenoside Rb1 alleviate hippocampus lesion induced by acute immobilization stress through regulating the BDNF mRNA and protein expressions in hippocampus.

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