2008•Journal of Shandong UniversityRequires access

Effect of NEP1-40 and GM-1 on hypoxic ischemic brain damage in newborn rats

Pingbo Yao

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Abstract

Objective To investigate the effects of NEP1-40 and GM-1 in newborn rats with hypoxic ischemic brain damage(HIBD).Methods 100 rats were randomly divided into 10 groups and five groups were treated in different ways at 6h: the normal control group,the sham-operation group,the HIBD model group,the GM-1 treatment group and the NEP1-40 treatment group,and the other five groups were treated at 24 h.Contents of Nogo-A mRNA in each group were determined by the method of in situ hybridization.Results The expression of Nogo-A mRNA in the HIBD groups was higher than that in the control groups,and was lower in the NEP1-40 groups than in the HIBD groups at both time points.There were no significant differences between the GM-1 group and the HIBD group when they were treated at 6h.However,the expression of Nogo-A mRNA was lower in the GM-1 group than in the HIBD group but was higher than the normal control group.Conclusion Nogo-A mRNA is significantly increased in newborn rats with HIBD.Nogo-A encoded by mRNA can inhibit the regeneration of the central nerve after injury,and NEP140 could antagonize the function and promotes the regeneration.GM-1 is also able to antagonize the expression of mRNA and stabilizes the cellular membrane,eases cellular edema of the injured nerve and accelerates the regeneration of new nerves.

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Objective To investigate the effects of NEP1-40 and GM-1 in newborn rats with hypoxic ischemic brain damage(HIBD).Methods 100 rats were randomly divided into 10 groups and five groups were treated in different ways at 6h: the normal control group,the sham-operation group,the HIBD model group,the GM-1 treatment group and the NEP1-40 treatment group,and the other five groups were treated at 24 h.Contents of Nogo-A mRNA in each group were determined by the method of in situ hybridization.Results The expression of Nogo-A mRNA in the HIBD groups was higher than that in the control groups,and was lower in the NEP1-40 groups than in the HIBD groups at both time points.There were no significant differences between the GM-1 group and the HIBD group when they were treated at 6h.However,the expression of Nogo-A mRNA was lower in the GM-1 group than in the HIBD group but was higher than the normal control group.Conclusion Nogo-A mRNA is significantly increased in newborn rats with HIBD.Nogo-A encoded by mRNA can inhibit the regeneration of the central nerve after injury,and NEP140 could antagonize the function and promotes the regeneration.GM-1 is also able to antagonize the expression of mRNA and stabilizes the cellular membrane,eases cellular edema of the injured nerve and accelerates the regeneration of new nerves.

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Available abstract

Objective To investigate the effects of NEP1-40 and GM-1 in newborn rats with hypoxic ischemic brain damage(HIBD).Methods 100 rats were randomly divided into 10 groups and five groups were treated in different ways at 6h: the normal control group,the sham-operation group,the HIBD model group,the GM-1 treatment group and the NEP1-40 treatment group,and the other five groups were treated at 24 h.Contents of Nogo-A mRNA in each group were determined by the method of in situ hybridization.Results The expression of Nogo-A mRNA in the HIBD groups was higher than that in the control groups,and was lower in the NEP1-40 groups than in the HIBD groups at both time points.There were no significant differences between the GM-1 group and the HIBD group when they were treated at 6h.However,the expression of Nogo-A mRNA was lower in the GM-1 group than in the HIBD group but was higher than the normal control group.Conclusion Nogo-A mRNA is significantly increased in newborn rats with HIBD.Nogo-A encoded by mRNA can inhibit the regeneration of the central nerve after injury,and NEP140 could antagonize the function and promotes the regeneration.GM-1 is also able to antagonize the expression of mRNA and stabilizes the cellular membrane,eases cellular edema of the injured nerve and accelerates the regeneration of new nerves.

Key concepts: Messenger RNA, Brain damage, In situ hybridization, Regeneration (biology), Biology, Internal medicine, Endocrinology, Andrology

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