Influence of ginsenoside on expression of brain-derived neurotrophic factor and receptor tyrosine ki

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:kdmasong
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BACKGROUND: It has been shown that ginsenoside, the effective component of ginseng, can enhance expression of choline acetyl transferase, as well as brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB), in cholinergic neurons of the basal forebrain. OBJECTIVE: To qualitatively and quantitatively verify the influence of ginsenoside on expression of BDNF and its receptor, TrkB, in the medial septum of aged rats, and to provide a molecular basis for clinical application. DESIGN, TIME AND SETTING: A contrast study, which was performed in the Department of Anatomy, China Medical University, and the Department of Anatomy, Shenyang Medical College between December 2005 and May 2007. MATERIALS: Thirty-five, healthy, female, Sprague Dawley rats were selected for this study. Ginsenoside (81% purity) was provided by Jilin Ji’an Wantai Chinese Medicine Factory; anti-BDNF antibody, anti-TrkB antibody, and their kits were provided by Wuhan Boster Company. METHODS: A total of 35 rats were divided into three groups: young (four months old), aging (26 months old), and ginsenoside. Rats in the ginsenoside group were administered ginsenoside (25 mg/kg/d) between 17 months and 26 months. MAIN OUTCOME MEASURES: Immunohistochemistry and in situ hybridization were used to measure expression of BDNF and TrkB in the medial septum of aged rats, and the detected results were expressed as gray values. RESULTS: ① Qualitative detection: using microscopy, degenerative neurons were visible in the medial septum in the aging group. However, neuronal morphology in the ginsenoside group was similar to neurons in the young group. ② Quantitative detection: the mean gray value of BDNF-positive and TrkB-positive products in the aging group were significantly higher than in the young group (t = 3.346, 4.169, P < 0.01); however, the mean gray value in the ginsenoside group was significantly lower than in the aging group (t = 2.432, 2.651, P < 0.01). CONCLUSION: Ginsenoside can increase expression of BDNF and TrkB in the medial septum and delay the natural degeneration in aged rats. BACKGROUND: It has been shown that ginsenoside, the effective component of ginseng, can enhance expression of choline acetyl transferase, as well as brain-derived neurotrophic factor (BDNF) and its receptor tyrosine kinase B (TrkB), in cholinergic neurons of the basal Forebrain. OBJECTIVE: To qualitatively and quantitatively verify the influence of ginsenoside on expression of BDNF and its receptor, TrkB, in the medial septum of aged rats, and to provide a molecular basis for clinical application. DESIGN, TIME AND SETTING: A contrast study , which was performed in the Department of Anatomy, China Medical University, and the Department of Anatomy, Shenyang Medical College between December 2005 and May 2007. MATERIALS: Thirty-five, healthy, female, Sprague Dawley rats were selected for this study. Ginsenoside (81% purity) was provided by Jilin Ji’an Wantai Chinese Medicine Factory; anti-BDNF antibody, anti-TrkB antibody, and their kits were provided by Wuhan Boster Company. METHODS: A t Otal of 35 rats were divided into three groups: young (four months old), aging (26 months old), and ginsenoside. Rats in the ginsenoside group were administered ginsenoside (25 mg/kg/d) between 17 months and 26 months. RESULTS: 1 Qualitative detection: using microscopy, The medial septum in the aging group. However, the neuronal morphology in the ginsenoside group was similar to neurons in the young group. 2 Quantitative detection: the mean gray value of BDNF-positive and TrkB-positive products in the aging group were significantly higher than In the young group (t = 3.346, 4.169, P < 0.01); however, the mean gray value in the ginsenoside group was significantly lower than in the aging group (t = 2.432, 2.651, P < 0.01). CONCLUSION: Ginsenosid e canIncrease expression of BDNF and TrkB in the medial septum and delay the natural degeneration in aged rats.
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