Objective To investigate whether the antioxidation and the regulation on the Extracellular Regulated Protein Kinases （ERK） signaling pathway are involved in the protective effects of blueberry on central nervous sys...Objective To investigate whether the antioxidation and the regulation on the Extracellular Regulated Protein Kinases （ERK） signaling pathway are involved in the protective effects of blueberry on central nervous system. Methods 30 Senescence-accelerated mice prone 8 （SAMP8） mice were divided into three groups and treated with normal diet, blueberry extracts （200 mg/kg.bw/day） and cyaniding-3-O-galactoside （Cy-3-GAL） （50 mg/kg.bw/day） from blueberry for 8 weeks. 10 SAMR1 mice were set as control group. The capacity of spatial memory was assessed by Passive avoidance task and Morris water maze. Histological analyses on hippocampus were completed. Malondialdehyde （MDA） levels, Superoxide Dismutase （SOD） activity and the expression of ERK were detected. Results Both Cy-3-GAL and blueberry extracts were shown effective functions to relieve cellular injury, improve hippocampal neurons survival and inhibit the pyramidal cell layer damage. Cy-3-GAL and blueberry extracts also increased SOD activity and reduced MDA content in brain tissues and plasma, and increased hippocampal phosphorylated ERK （p-ERK） expression in SAMP8 mice. Further more, the passive avoidance task test showed that both the latency time and the number of errors were improved by Cy-3-GAL treatment, and the Morris Water Maze test showed significant decreases of latency were detected by Cy-3-GAL and blueberry extracts treatment on day 4. Conclusion Blueberry extracts may reverse the declines of cognitive and behavioral function in the ageing process through several pathways, including enhancing the capacity of antioxidation, altering stress signaling. Cy-3-GAL may be an important active ingredient for these biological effects.展开更多
BACKGROUND： Along with aging, antioxidase activity decreases and oxygen-derived free radicals greatly accumulate, resulting in cellular senescence, or even cell death. This is manifested by hypomnesia and disordered ...BACKGROUND： Along with aging, antioxidase activity decreases and oxygen-derived free radicals greatly accumulate, resulting in cellular senescence, or even cell death. This is manifested by hypomnesia and disordered metabolism of free radicals. Studies have reported that Longyanshen polysaccharides have the function of antioxidation and improved brain memory. OBJECTIVE： To observe the effects of Longyanshen polysaccharides on free radical metabolism in brain tissue to verify the anti-aging mechanisms in senescence accelerated-prone （SAMP8） mice. DESIGN, TIME AND SETTING： The randomized, controlled, biochemical experiment was performed in the Department of Pharmacology and Scientific Experimental Center of Guangxi Medical University （China） from September 2005 to January 2008. MATERIALS： Forty SAMP8 mice were randomized into four groups： SAMP8 control group, as well as low-, mid-, and high-dose polysaccharide, with 10 mice in each group. Ten senescence accelerated-resistantprone （SAMR 1） mice served as the normal control group. Longyanshen polysaccharides, extracted from the medical plant Longyanshen, were supplied by the Department of Pharmacology, Guangxi Medical University Superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, malonaldehyde （MDA）, nitric oxide （NO）, and total protein test kitwere purchased from Nanjing Jiancheng Bioengineering Institute （China）. METHODS： SAMP8 mice were used to establish a dementia animal model. SAMP8 and SAMR1 control mice were administered 30 mL/kg saline. The low-, middle-, and high-dose polysaccharide groups were administered 45, 90, and 180 mg/kg Longyanshen polysaccharides, respectively. Each group was treated by intragastric administration, once daily, for 50 continuous days. MAIN OUTCOME MEASURES： One hour after the last administration, mouse brain tissues were collected, and retro orbital blood sampling was performed. Spectrophotometry was used to measure SOD and GSH-Px activity, as well as MDA and NO concentration in sera and brains of SAMP8 mice. RESULTS： SOD and GSH-Px activity decreased significantly, and MDA and NO concentration increased significantly, in SAMP8 control group brain tissues, compared with the SAMP1 control group （P 〈 0.05）. Compared with the SAMP8 control group, Longyanshen polysaccharide-treated groups exhibited enhanced SOD and GSH-Px activity, as well as decreased MDA and NO concentration, in serum and brain tissue （P 〈 0.05）. Longyanshen polysaccharides exerted a similar effect on SOD, GSH-Px, MDA, and NO concentrations in serum and brain tissues of SAMP8 mice. CONCLUSION： Longyanshen polysaccharides scavenged free radicals effectively, reduced NO concentration and ameliorated NO toxicity, thereby influenced aging and stress, as well as improving memory capacity in the brain.展开更多
Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8...Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.展开更多
基金supported by the grant of National Natural Science Foundation of Tianjin(09JCYBJC12900)
文摘Objective To investigate whether the antioxidation and the regulation on the Extracellular Regulated Protein Kinases （ERK） signaling pathway are involved in the protective effects of blueberry on central nervous system. Methods 30 Senescence-accelerated mice prone 8 （SAMP8） mice were divided into three groups and treated with normal diet, blueberry extracts （200 mg/kg.bw/day） and cyaniding-3-O-galactoside （Cy-3-GAL） （50 mg/kg.bw/day） from blueberry for 8 weeks. 10 SAMR1 mice were set as control group. The capacity of spatial memory was assessed by Passive avoidance task and Morris water maze. Histological analyses on hippocampus were completed. Malondialdehyde （MDA） levels, Superoxide Dismutase （SOD） activity and the expression of ERK were detected. Results Both Cy-3-GAL and blueberry extracts were shown effective functions to relieve cellular injury, improve hippocampal neurons survival and inhibit the pyramidal cell layer damage. Cy-3-GAL and blueberry extracts also increased SOD activity and reduced MDA content in brain tissues and plasma, and increased hippocampal phosphorylated ERK （p-ERK） expression in SAMP8 mice. Further more, the passive avoidance task test showed that both the latency time and the number of errors were improved by Cy-3-GAL treatment, and the Morris Water Maze test showed significant decreases of latency were detected by Cy-3-GAL and blueberry extracts treatment on day 4. Conclusion Blueberry extracts may reverse the declines of cognitive and behavioral function in the ageing process through several pathways, including enhancing the capacity of antioxidation, altering stress signaling. Cy-3-GAL may be an important active ingredient for these biological effects.
基金Supported by: Guangxi Natural Science Foundation, No. 0447030Guangxi Scientific Research and Technological Development Projects, No. 0630002-2A
文摘BACKGROUND： Along with aging, antioxidase activity decreases and oxygen-derived free radicals greatly accumulate, resulting in cellular senescence, or even cell death. This is manifested by hypomnesia and disordered metabolism of free radicals. Studies have reported that Longyanshen polysaccharides have the function of antioxidation and improved brain memory. OBJECTIVE： To observe the effects of Longyanshen polysaccharides on free radical metabolism in brain tissue to verify the anti-aging mechanisms in senescence accelerated-prone （SAMP8） mice. DESIGN, TIME AND SETTING： The randomized, controlled, biochemical experiment was performed in the Department of Pharmacology and Scientific Experimental Center of Guangxi Medical University （China） from September 2005 to January 2008. MATERIALS： Forty SAMP8 mice were randomized into four groups： SAMP8 control group, as well as low-, mid-, and high-dose polysaccharide, with 10 mice in each group. Ten senescence accelerated-resistantprone （SAMR 1） mice served as the normal control group. Longyanshen polysaccharides, extracted from the medical plant Longyanshen, were supplied by the Department of Pharmacology, Guangxi Medical University Superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, malonaldehyde （MDA）, nitric oxide （NO）, and total protein test kitwere purchased from Nanjing Jiancheng Bioengineering Institute （China）. METHODS： SAMP8 mice were used to establish a dementia animal model. SAMP8 and SAMR1 control mice were administered 30 mL/kg saline. The low-, middle-, and high-dose polysaccharide groups were administered 45, 90, and 180 mg/kg Longyanshen polysaccharides, respectively. Each group was treated by intragastric administration, once daily, for 50 continuous days. MAIN OUTCOME MEASURES： One hour after the last administration, mouse brain tissues were collected, and retro orbital blood sampling was performed. Spectrophotometry was used to measure SOD and GSH-Px activity, as well as MDA and NO concentration in sera and brains of SAMP8 mice. RESULTS： SOD and GSH-Px activity decreased significantly, and MDA and NO concentration increased significantly, in SAMP8 control group brain tissues, compared with the SAMP1 control group （P 〈 0.05）. Compared with the SAMP8 control group, Longyanshen polysaccharide-treated groups exhibited enhanced SOD and GSH-Px activity, as well as decreased MDA and NO concentration, in serum and brain tissue （P 〈 0.05）. Longyanshen polysaccharides exerted a similar effect on SOD, GSH-Px, MDA, and NO concentrations in serum and brain tissues of SAMP8 mice. CONCLUSION： Longyanshen polysaccharides scavenged free radicals effectively, reduced NO concentration and ameliorated NO toxicity, thereby influenced aging and stress, as well as improving memory capacity in the brain.
基金Supported by the National Natureal Science Foundation of China(No.30701121)
文摘Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.
