Neurological research · 2011
Bone marrow mesenchymal stem cells can improve the motor function of a Huntington's disease rat model.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Jiang Yufeng, Lv Hailong, Huang Shanshan, Tan Huiping, Zhang Yinong, Li He
Аннотация
OBJECTIVES: The purpose of this study was to investigate the ability of bone marrow mesenchymal stem cells (BMSCs) to survive in the striatum and improve motor function in the quinolinic acid (QA) lesion rat model of Huntington's disease (HD).
METHODS: One week following QA lesioning of the striatum, rats were transplanted with BMSCs that had been expanded in culture and labeled with 4'-6-diamidino-2-phenylindole (DAPI) prior to transplantation.
RESULTS: BMSCs survived transplantation into the lesioned striatum and differentiated into both neurons. Moreover, transplantation of BMSCs significantly reduced motor dysfunction observed following striatal QA lesioning. Stereological striatal volume analyses performed on Nissl-stained sections revealed that rats transplanted with BMSCs had a greater striatal volume on the lesioned side compared with rats injected with vehicle. Cultured BMSCs expressed trophic factors, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and ciliary neurotrophic factor (CNTF). In the striatum of BMSC-treated group, the expression levels of these genes were significantly elevated when compared with those of the control group.
CONCLUSION: Our data suggested that striatal transplants of BMSCs elicit behavioral and anatomical recovery in the QA lesion model of HD.
METHODS: One week following QA lesioning of the striatum, rats were transplanted with BMSCs that had been expanded in culture and labeled with 4'-6-diamidino-2-phenylindole (DAPI) prior to transplantation.
RESULTS: BMSCs survived transplantation into the lesioned striatum and differentiated into both neurons. Moreover, transplantation of BMSCs significantly reduced motor dysfunction observed following striatal QA lesioning. Stereological striatal volume analyses performed on Nissl-stained sections revealed that rats transplanted with BMSCs had a greater striatal volume on the lesioned side compared with rats injected with vehicle. Cultured BMSCs expressed trophic factors, including nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), glial cell line-derived neurotrophic factor (GDNF) and ciliary neurotrophic factor (CNTF). In the striatum of BMSC-treated group, the expression levels of these genes were significantly elevated when compared with those of the control group.
CONCLUSION: Our data suggested that striatal transplants of BMSCs elicit behavioral and anatomical recovery in the QA lesion model of HD.