OBJECTIVE To research the effect of Rhodiolae on cognitive function on dementia rats and to investigate its potential mechanism.METHODS Established dementia model via injecting ibotenic acid into basal nuclei,and rand...OBJECTIVE To research the effect of Rhodiolae on cognitive function on dementia rats and to investigate its potential mechanism.METHODS Established dementia model via injecting ibotenic acid into basal nuclei,and randomly divided the model rats into model group,Aricept group(1.4 mg·kg-1)and Rhodiolae group(0.14 mg·kg-1),moreover the sham group was built byinjecting normal saline.All animals received homologous drugs after modeling 1 week,and the sham group and model group were gave isometric normal saline(10 mL·kg-1),1/d.Morris water maze was used to evaluate the change of cognitive function after the rats were treated 40 d,and pathomorphism in CA1 and cerebral cortex were observed by Nissl staining and the numbers of nerve cell in these areas were counted.The concentration of MDA,H2O2,CAT,SOD and GR in brain tissue were detected by spectrophotography.RESULTS Compared to model group,the escape latency of Rhodiolae groups〔(31.10±20.97)s compare to(51.07±13.04)s〕was shortened but it hadn′t statistical difference,and the total swimming distance〔(8469.88±4724.74)cm compare to(15862.17±1315.69)cm〕was shortened obviously,furthermore the times entered the target quadrant〔(9.50±1.87)times compare to(6.50±1.38)times〕and the percentage in target quadrant〔(33.87±4.47)%compare to(26.17±2.58)%〕were evidently increased.Moderate shrinkage of nucleus of neurons in cerebral cortex of model rats,mild hyperplasia of glial cells and loosely neuron was also observed in CA1 area,but those lesions were distinctly ameliorated in Rhodiolae groups.What′s more,the numbers of nerve cells in CA1〔(70.40±4.00)compare to(45.50±4.95)〕and cerebral cortex〔(63.00±5.29)compare to(42.40±11.87)〕of Rhodiolae groups were obviously increased.In addition,compared to model group,the content of MDA〔(14.72±4.42)compare to(19.99±4.70)g protein·L-1〕and H2O2〔(60.07±6.38)mmol·L-1compare to(76.37±6.06)mmol·L-1〕were evidently decreased,the activity of GSH〔(41.30±14.81)k U·g-1protein compare to(15.93±3.59)k U·g-1protein〕was visibly increased,and the activity of SOD〔(5.74±3.76)g protein·L-1compare to(2.72±1.09)g protein·L-1〕and CAT〔(210.45±60.11)k U·g-1protein compare to(171.48±56.50)k U·g-1protein〕were also increased but without statistical difference.CONCLUSION Rhodiolae improve learning and remembering function,ameliorate pathological changes and protect neuronal loss which respond to decrease the oxidative products and enhance the activity of antioxidase.展开更多
目的观察鹅膏蕈氨酸对大鼠海马神经元的毒性作用,探讨鹅膏蕈氨酸的毒理学机制。方法成年Wistar雄性大鼠,侧脑室1次性注射鹅膏蕈氨酸(Ibotenic acid,IBO)(每侧注射5μl)。10 d后,利用苏木素-伊红(hematoxylin and eosin,HE)染色、电镜技...目的观察鹅膏蕈氨酸对大鼠海马神经元的毒性作用,探讨鹅膏蕈氨酸的毒理学机制。方法成年Wistar雄性大鼠,侧脑室1次性注射鹅膏蕈氨酸(Ibotenic acid,IBO)(每侧注射5μl)。10 d后,利用苏木素-伊红(hematoxylin and eosin,HE)染色、电镜技术、原位杂交、免疫组化染色等方法,观察大鼠海马神经元、淀粉样前体蛋白(β-amyloid protein precursor,APP)基因表达水平及β-淀粉样蛋白(β-amyloid protein,Aβ)含量的变化。结果侧脑室注射鹅膏蕈氨酸,能导致大鼠海马神经元变性、缺失;APP基因表达水平明显升高,Aβ生成增多。结论上调APP基因表达水平,使Aβ生成增多,可能是鹅膏蕈氨酸导致大鼠海马神经元损害的毒理学机制之一。展开更多
基金The project supported by Key Projects of National Natural Science Foundation of China(81430100)Academic and technical leaders of Sichuan Province to Raise Funds for Funding Projects(2015058)Sichuan Province Youth Science and technology Innovation Research Team(2014TD0007)
文摘OBJECTIVE To research the effect of Rhodiolae on cognitive function on dementia rats and to investigate its potential mechanism.METHODS Established dementia model via injecting ibotenic acid into basal nuclei,and randomly divided the model rats into model group,Aricept group(1.4 mg·kg-1)and Rhodiolae group(0.14 mg·kg-1),moreover the sham group was built byinjecting normal saline.All animals received homologous drugs after modeling 1 week,and the sham group and model group were gave isometric normal saline(10 mL·kg-1),1/d.Morris water maze was used to evaluate the change of cognitive function after the rats were treated 40 d,and pathomorphism in CA1 and cerebral cortex were observed by Nissl staining and the numbers of nerve cell in these areas were counted.The concentration of MDA,H2O2,CAT,SOD and GR in brain tissue were detected by spectrophotography.RESULTS Compared to model group,the escape latency of Rhodiolae groups〔(31.10±20.97)s compare to(51.07±13.04)s〕was shortened but it hadn′t statistical difference,and the total swimming distance〔(8469.88±4724.74)cm compare to(15862.17±1315.69)cm〕was shortened obviously,furthermore the times entered the target quadrant〔(9.50±1.87)times compare to(6.50±1.38)times〕and the percentage in target quadrant〔(33.87±4.47)%compare to(26.17±2.58)%〕were evidently increased.Moderate shrinkage of nucleus of neurons in cerebral cortex of model rats,mild hyperplasia of glial cells and loosely neuron was also observed in CA1 area,but those lesions were distinctly ameliorated in Rhodiolae groups.What′s more,the numbers of nerve cells in CA1〔(70.40±4.00)compare to(45.50±4.95)〕and cerebral cortex〔(63.00±5.29)compare to(42.40±11.87)〕of Rhodiolae groups were obviously increased.In addition,compared to model group,the content of MDA〔(14.72±4.42)compare to(19.99±4.70)g protein·L-1〕and H2O2〔(60.07±6.38)mmol·L-1compare to(76.37±6.06)mmol·L-1〕were evidently decreased,the activity of GSH〔(41.30±14.81)k U·g-1protein compare to(15.93±3.59)k U·g-1protein〕was visibly increased,and the activity of SOD〔(5.74±3.76)g protein·L-1compare to(2.72±1.09)g protein·L-1〕and CAT〔(210.45±60.11)k U·g-1protein compare to(171.48±56.50)k U·g-1protein〕were also increased but without statistical difference.CONCLUSION Rhodiolae improve learning and remembering function,ameliorate pathological changes and protect neuronal loss which respond to decrease the oxidative products and enhance the activity of antioxidase.
文摘目的观察鹅膏蕈氨酸对大鼠海马神经元的毒性作用,探讨鹅膏蕈氨酸的毒理学机制。方法成年Wistar雄性大鼠,侧脑室1次性注射鹅膏蕈氨酸(Ibotenic acid,IBO)(每侧注射5μl)。10 d后,利用苏木素-伊红(hematoxylin and eosin,HE)染色、电镜技术、原位杂交、免疫组化染色等方法,观察大鼠海马神经元、淀粉样前体蛋白(β-amyloid protein precursor,APP)基因表达水平及β-淀粉样蛋白(β-amyloid protein,Aβ)含量的变化。结果侧脑室注射鹅膏蕈氨酸,能导致大鼠海马神经元变性、缺失;APP基因表达水平明显升高,Aβ生成增多。结论上调APP基因表达水平,使Aβ生成增多,可能是鹅膏蕈氨酸导致大鼠海马神经元损害的毒理学机制之一。
