Objective To investigate the role of D-galactose, especially in the structural and functional changes of the immune system in aging. Methods Serum levels of advanced glycation end-products （AGE） were determined by E...Objective To investigate the role of D-galactose, especially in the structural and functional changes of the immune system in aging. Methods Serum levels of advanced glycation end-products （AGE） were determined by ELISA method. Ultra-structures of thymus and spleen were detected by transmission electron microscopy. MTT method was used to determine the lymphocyte proliferation. IL-2 activity was determined by bioassay. Northern blot was used to detect the IL-2 mRNA levels. Results Serum AGE levels of D-galactose- （P〈0.01） and AGE-treated （P〈0.05） mice （n=8） were increased significantly. The ultra-structures of thymus and spleen in D-galactose- and AGE-treated mice showed regressive changes similar to those in the aged control group. The lymphocyte mitogenesis and IL-2 activity of spleen were also decreased significantly （P〈0.01, n=8）. The change of IL-2 activity shown by Northern blot resulted from the change of mRNA expression. The AGE plus aminoguanidine group, however, showed no significant change in these parameters in comparison with the young control group （P〈0.01 or P〈0.05, n=8）. Conclusion D-galactose and AGE lead to a mimic regression change of aging in the immune system in vivo.展开更多
Standardized Ginkgo biloba leaf extract has been used in clinical trials for its beneficial effects on brain func- tions, particularly in dementia. Substantial experimental evidences indicated that Ginkgo biloba leaf ...Standardized Ginkgo biloba leaf extract has been used in clinical trials for its beneficial effects on brain func- tions, particularly in dementia. Substantial experimental evidences indicated that Ginkgo biloba leaf extract （EGB） protected neuronal cells from a variety of insults. We investigated the effect of EGB on cognitive ability and protein kinase B （PKB） activity in hippocampal neuronal cells of dementia model rats. Rats received an intra- peritoneal injection of D-galactose to induce dementia. Forty-eight Spraque-Dawley rats were randomly divided into six groups, including the control group, D-galactose group （Gal）, low-dose EGB group （EGB-L）, mid-dose EGB group （EGB-M）, high-dose EGB group （EGB-H） and treatment group. The EGB-L, EGB-M and EGB-H groups were administered with EGB and D-galactose simultaneously. Y-maze, cresyl violet staining, TUNEL assays and immunohistochemistry staining were performed to detect learning and memory abilities, morpho- logical changes in the hippocampus, neuronal apoptosis and the expressing level of phospho-PKB, respectively. Rats in the Gal group showed decreased abilities of learning and memory, and hippocampal pyramidal cell layer was damaged, while EGB administration improved learning and memory abilities. The Gal group exhibited many stained, condensed nuclei and micronuclei, either isolated or within the cytoplasm of cells （39.5 ± 1.4）. Apoptotic cells decreased in the groups of EGB-L （35.9±0.9）, EGB-M （16.8± 1.0） and EGB-H （10.1±0.8）, and there were statistical significances compared with the Gal group. Immunoreactivity of phospho-PKB was localized diffusely throughout the cytosol of cells in all groups, while the immunoreactivity of the Gal group was weak. EGB signifi- cantly attenuated learning and memory impairment in a dose-dependent manner, while it could decrease the nmber of TUNEL-positive cells, and increase the activity of PKB. Our results demonstrated that EGB attenuated memory impairment and cell apoptosis in galactose-induced dementia model rats by activating PKB.展开更多
Objective It has been reported that D-galactose （D-gal） can model subacute aging, and aluminum （AI） acts as a neurotoxin, but combined effects of them have not been reported. The present work aimed to reveal the e...Objective It has been reported that D-galactose （D-gal） can model subacute aging, and aluminum （AI） acts as a neurotoxin, but combined effects of them have not been reported. The present work aimed to reveal the effect of combined administration of D-gal and A1 in mice and compare the effect of D-gal treatment with that of A1 treatment. Meth- ods A1 was intragastricaHy administered and D-gal was subcutaneously injected into Kunming mice for 10 consecutive weeks. Learning and memory, eholinergic systems, as well as protein levels of amyloid β （Aβ） and hyperphosphorylated tau were determined using Morri water maze test, biochemical assays and immunohistochemical staining, respectively. Results The mice with combined treatment had obvious learning and memory deficits, and showed decreases in brain ace- tylcholine （ACh） level and in activities of choline acetyltransferase （CHAT） and acetyleholinesterase （ACHE）. Formation of senile plaque （SP）-like and neurofibrillary tangle （NFT）-like structures was also observed. The behavioral and pathologi- cal changes persisted for at least 6 weeks after withdrawal of D-gal and A1. Conclusion Combined use of D-gal and A1 is an effective way to establish the non-transgenic Alzheimer＇s disease （AD） animal model, and is useful for studies of AD pathogenesis and therapeutic evaluation.展开更多
The study aims to investigate the repair effects of Ser-Ser-Asp-Ala-Phe-Phe-Pro-Phe-Arg(SSDAFFPFR)and Ser-Asn-Val-Phe-Asp-Met-Phe(SNVFDMF)peptides on scopolamine-caused memory impairment in mice.Behavioral experiments...The study aims to investigate the repair effects of Ser-Ser-Asp-Ala-Phe-Phe-Pro-Phe-Arg(SSDAFFPFR)and Ser-Asn-Val-Phe-Asp-Met-Phe(SNVFDMF)peptides on scopolamine-caused memory impairment in mice.Behavioral experiments have revealed that Antarctic krill peptides can ameliorate scopolamine caused memory impairment by changing the behavior of mice.In comparison with the scopolamine group,the two peptides at a dose of 40 mg/kg could improve memory impairment.The serum SOD activity(82.82±0.19 vs 79.47±2.42 U/mg prot)and hippocampal ACh level(101.46±3.23 vs 99.85±7.13μg/mg prot)of SSDAFFPFR were higher than those of SNVFDMF.Hippocampal AChE activity(0.20±0.03 vs 0.53±0.02 U/mg prot),hippocampal MDA level(1.56±0.01 vs 1.63±0.05 nmol/mg prot)and the serum MDA level(3.38±0.24 vs 3.88±0.21 nmol/mg prot)was lower than that of SNVFDMF.The state of mouse hippocampal cells was further observed by a microscopic imaging system.In addition,western blot analysis showed that SSDAFFPFR could significantly inhibit the expression of Bax,caspase-3,and p53,and promote the expression of BCL-XL,CREB,and BDNF,thus protecting hippocampal neurons in mice.In conclusion,the Antarctic krill peptide can repair scopolamine-induced memory impairment in mice.展开更多
基金This work was supported by a grant from the Major State Basic Research Development Program Foundation of China (No. 2007CB507406) and a grant from the National Natural Science Foundation of China (No. 30600659).
文摘Objective To investigate the role of D-galactose, especially in the structural and functional changes of the immune system in aging. Methods Serum levels of advanced glycation end-products （AGE） were determined by ELISA method. Ultra-structures of thymus and spleen were detected by transmission electron microscopy. MTT method was used to determine the lymphocyte proliferation. IL-2 activity was determined by bioassay. Northern blot was used to detect the IL-2 mRNA levels. Results Serum AGE levels of D-galactose- （P〈0.01） and AGE-treated （P〈0.05） mice （n=8） were increased significantly. The ultra-structures of thymus and spleen in D-galactose- and AGE-treated mice showed regressive changes similar to those in the aged control group. The lymphocyte mitogenesis and IL-2 activity of spleen were also decreased significantly （P〈0.01, n=8）. The change of IL-2 activity shown by Northern blot resulted from the change of mRNA expression. The AGE plus aminoguanidine group, however, showed no significant change in these parameters in comparison with the young control group （P〈0.01 or P〈0.05, n=8）. Conclusion D-galactose and AGE lead to a mimic regression change of aging in the immune system in vivo.
文摘Standardized Ginkgo biloba leaf extract has been used in clinical trials for its beneficial effects on brain func- tions, particularly in dementia. Substantial experimental evidences indicated that Ginkgo biloba leaf extract （EGB） protected neuronal cells from a variety of insults. We investigated the effect of EGB on cognitive ability and protein kinase B （PKB） activity in hippocampal neuronal cells of dementia model rats. Rats received an intra- peritoneal injection of D-galactose to induce dementia. Forty-eight Spraque-Dawley rats were randomly divided into six groups, including the control group, D-galactose group （Gal）, low-dose EGB group （EGB-L）, mid-dose EGB group （EGB-M）, high-dose EGB group （EGB-H） and treatment group. The EGB-L, EGB-M and EGB-H groups were administered with EGB and D-galactose simultaneously. Y-maze, cresyl violet staining, TUNEL assays and immunohistochemistry staining were performed to detect learning and memory abilities, morpho- logical changes in the hippocampus, neuronal apoptosis and the expressing level of phospho-PKB, respectively. Rats in the Gal group showed decreased abilities of learning and memory, and hippocampal pyramidal cell layer was damaged, while EGB administration improved learning and memory abilities. The Gal group exhibited many stained, condensed nuclei and micronuclei, either isolated or within the cytoplasm of cells （39.5 ± 1.4）. Apoptotic cells decreased in the groups of EGB-L （35.9±0.9）, EGB-M （16.8± 1.0） and EGB-H （10.1±0.8）, and there were statistical significances compared with the Gal group. Immunoreactivity of phospho-PKB was localized diffusely throughout the cytosol of cells in all groups, while the immunoreactivity of the Gal group was weak. EGB signifi- cantly attenuated learning and memory impairment in a dose-dependent manner, while it could decrease the nmber of TUNEL-positive cells, and increase the activity of PKB. Our results demonstrated that EGB attenuated memory impairment and cell apoptosis in galactose-induced dementia model rats by activating PKB.
基金supported by National Natural Science Foundation of China (No. 30271502)
文摘Objective It has been reported that D-galactose （D-gal） can model subacute aging, and aluminum （AI） acts as a neurotoxin, but combined effects of them have not been reported. The present work aimed to reveal the effect of combined administration of D-gal and A1 in mice and compare the effect of D-gal treatment with that of A1 treatment. Meth- ods A1 was intragastricaHy administered and D-gal was subcutaneously injected into Kunming mice for 10 consecutive weeks. Learning and memory, eholinergic systems, as well as protein levels of amyloid β （Aβ） and hyperphosphorylated tau were determined using Morri water maze test, biochemical assays and immunohistochemical staining, respectively. Results The mice with combined treatment had obvious learning and memory deficits, and showed decreases in brain ace- tylcholine （ACh） level and in activities of choline acetyltransferase （CHAT） and acetyleholinesterase （ACHE）. Formation of senile plaque （SP）-like and neurofibrillary tangle （NFT）-like structures was also observed. The behavioral and pathologi- cal changes persisted for at least 6 weeks after withdrawal of D-gal and A1. Conclusion Combined use of D-gal and A1 is an effective way to establish the non-transgenic Alzheimer＇s disease （AD） animal model, and is useful for studies of AD pathogenesis and therapeutic evaluation.
基金supported by National Natural Science Foundation of China[Grant No.32022067]Dalian Hih-level Talent Innovation Support Program of China[Grant No.2019RQ003].
文摘The study aims to investigate the repair effects of Ser-Ser-Asp-Ala-Phe-Phe-Pro-Phe-Arg(SSDAFFPFR)and Ser-Asn-Val-Phe-Asp-Met-Phe(SNVFDMF)peptides on scopolamine-caused memory impairment in mice.Behavioral experiments have revealed that Antarctic krill peptides can ameliorate scopolamine caused memory impairment by changing the behavior of mice.In comparison with the scopolamine group,the two peptides at a dose of 40 mg/kg could improve memory impairment.The serum SOD activity(82.82±0.19 vs 79.47±2.42 U/mg prot)and hippocampal ACh level(101.46±3.23 vs 99.85±7.13μg/mg prot)of SSDAFFPFR were higher than those of SNVFDMF.Hippocampal AChE activity(0.20±0.03 vs 0.53±0.02 U/mg prot),hippocampal MDA level(1.56±0.01 vs 1.63±0.05 nmol/mg prot)and the serum MDA level(3.38±0.24 vs 3.88±0.21 nmol/mg prot)was lower than that of SNVFDMF.The state of mouse hippocampal cells was further observed by a microscopic imaging system.In addition,western blot analysis showed that SSDAFFPFR could significantly inhibit the expression of Bax,caspase-3,and p53,and promote the expression of BCL-XL,CREB,and BDNF,thus protecting hippocampal neurons in mice.In conclusion,the Antarctic krill peptide can repair scopolamine-induced memory impairment in mice.
