Objective To investigate the role of myelin protein zero （P 0） in 2,5-hexanedione （2,5-HD）-induced peripheral nerve injury,and the protective effect of Ginkgo biloba extract （Egb761） on 2,5-HD-induced toxic peri...Objective To investigate the role of myelin protein zero （P 0） in 2,5-hexanedione （2,5-HD）-induced peripheral nerve injury,and the protective effect of Ginkgo biloba extract （Egb761） on 2,5-HD-induced toxic peripheral neuropathy.Methods After 4 weeks of treatment with 2,5-HD at different doses （50,100,200,400 mg/kg） in rats,changes in the levels of P 0 in rat sciatic nerves was investigated,and the effect of Egb761 on 2,5-HD-induced toxic peripheral neuropathy was studied.Results The blood-nerve barrier （BNB） permeability of the sciatic nerve increased,and the expression of P 0 mRNA and P 0 protein decreased in a dose-dependent manner after treatment with 2,5-HD for 4 weeks.Pretreatment with Egb761 protected against BNB interruption,and inhibited P 0 mRNA and protein reduction during 2,5-HD treatment.Pretreatment with Egb761 significantly reduced loss of body weight （P0.01） and mitigated gait abnormalities （2.85±0.22） induced by 400 mg/kg 2,5-HD （P0.01）.It also reduced the signs of neurotoxicity induced by 2,5-HD.Conclusion 2,5-HD inhibited the expression of P 0 in a dose-dependent manner,and this may be an important mechanism by which toxic peripheral neuropathy is induced by 2,5-HD.Egb761 has a protective effect against 2,5-HD-induced peripheral neurotoxicity in rats.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
Previous studies have demonstrated a neuroprotective effect of extract of Ginkgo biloba against neuronal damage, but have mainly focused on antioxidation of extract of Ginkgo biloba. To date, limited studies have dete...Previous studies have demonstrated a neuroprotective effect of extract of Ginkgo biloba against neuronal damage, but have mainly focused on antioxidation of extract of Ginkgo biloba. To date, limited studies have determined whether extrasct of Ginkgo biloba has a protective effect on neuronal damage. In the present study, acrylamide and 30, 60, and 120 mg/kg extract of Ginkgo biloba were administered for 4 weeks by gavage to establish mouse models. Our results showed that 30, 60, and 120 mg/kg extract of Ginkgo biloba effectively alleviated the abnormal gait of poisoned mice, and up-regulated protein expression levels of doublecortin（DCX）, brain-derived neurotrophic factor, and growth associated protein-43（GAP-43） in the hippocampus. Simultaneously, DCX-and GAP-43-immunoreactive cells increased. These findings suggest that extract of Ginkgo biloba can mitigate neurotoxicity induced by acrylamide, and thereby promote neuronal regeneration in the hippocampus of acrylamide-treated mice.展开更多
基金supported by the National Nature Science Foundation of China (No.30700674 and No.30625031)the Project for Technologies of Occupational Health Surveillance and Detection (200902006)the Youth Fund of Chinese Center of Disease Control (2010A204)
文摘Objective To investigate the role of myelin protein zero （P 0） in 2,5-hexanedione （2,5-HD）-induced peripheral nerve injury,and the protective effect of Ginkgo biloba extract （Egb761） on 2,5-HD-induced toxic peripheral neuropathy.Methods After 4 weeks of treatment with 2,5-HD at different doses （50,100,200,400 mg/kg） in rats,changes in the levels of P 0 in rat sciatic nerves was investigated,and the effect of Egb761 on 2,5-HD-induced toxic peripheral neuropathy was studied.Results The blood-nerve barrier （BNB） permeability of the sciatic nerve increased,and the expression of P 0 mRNA and P 0 protein decreased in a dose-dependent manner after treatment with 2,5-HD for 4 weeks.Pretreatment with Egb761 protected against BNB interruption,and inhibited P 0 mRNA and protein reduction during 2,5-HD treatment.Pretreatment with Egb761 significantly reduced loss of body weight （P0.01） and mitigated gait abnormalities （2.85±0.22） induced by 400 mg/kg 2,5-HD （P0.01）.It also reduced the signs of neurotoxicity induced by 2,5-HD.Conclusion 2,5-HD inhibited the expression of P 0 in a dose-dependent manner,and this may be an important mechanism by which toxic peripheral neuropathy is induced by 2,5-HD.Egb761 has a protective effect against 2,5-HD-induced peripheral neurotoxicity in rats.
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 the Natural Science Foundation of Guangdong Province of China,No.2014A030310455the Pearl River S&T Nova Program Foundation of Guangzhou City of China,No.201710010002
文摘Previous studies have demonstrated a neuroprotective effect of extract of Ginkgo biloba against neuronal damage, but have mainly focused on antioxidation of extract of Ginkgo biloba. To date, limited studies have determined whether extrasct of Ginkgo biloba has a protective effect on neuronal damage. In the present study, acrylamide and 30, 60, and 120 mg/kg extract of Ginkgo biloba were administered for 4 weeks by gavage to establish mouse models. Our results showed that 30, 60, and 120 mg/kg extract of Ginkgo biloba effectively alleviated the abnormal gait of poisoned mice, and up-regulated protein expression levels of doublecortin（DCX）, brain-derived neurotrophic factor, and growth associated protein-43（GAP-43） in the hippocampus. Simultaneously, DCX-and GAP-43-immunoreactive cells increased. These findings suggest that extract of Ginkgo biloba can mitigate neurotoxicity induced by acrylamide, and thereby promote neuronal regeneration in the hippocampus of acrylamide-treated mice.
