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1.
China Journal of Chinese Materia Medica ; (24): 407-411, 2014.
Artigo em Chinês | WPRIM | ID: wpr-287574

RESUMO

Neural stem cells in brains have capacities of proliferation and differentiation, which is very critical to rebuild the cerebral cortex functions. Therefore, it is of great importance to find key targets and network pathways that regulate the proliferation of neural stem cells, which is also a pressing problem in the medical circle. With the Notch pathway as the core of the network, this paper summarized the advance of the bimolecular network system composed of Wnt, Shh, EGFR, cytokines and Notch signal, and analyzed such key nodes as Notch receptor, CBF1, NICD, Hesl, which may become potential targets of new-type drugs in the future. With the multi-component, multi-target, multi-lever characteristics, traditional Chinese medicines have many common grounds with the network pharmacology. The active component groups or active ingredients in traditional Chinese medicines are one of the material bases for showing their network pharmacological effect, which is worth exploring. This paper aims to provide a new strategy for the treatment of neurodegenerative disease and nerve injury with traditional Chinese medicines.


Assuntos
Animais , Humanos , Proliferação de Células , Células-Tronco Neurais , Biologia Celular , Metabolismo , Transdução de Sinais , Biologia de Sistemas
2.
China Journal of Chinese Materia Medica ; (24): 3776-3781, 2013.
Artigo em Chinês | WPRIM | ID: wpr-291285

RESUMO

The neural stem cells (NSCs), play a crucial role in stroke treatment, which can be regulated by a few of traditional Chinese medicines. In this study, the effect of the Mongolian medicine Baimai powder effective compounds group (BMECG) on the proliferation of NSCs has been investigated. The cultured NSCs which were isolated from newborn rat cerebral cortical in vitro were exposed to oxygen glucose deprivation/reoxgenation (OGD/R). The CFSE immunofluorescence staining was employed to identify the proliferation of NSCs by flow cytometry. Furthermore, the bilateral carotid artery occlusion (BCAO) was established on Kunming mice, and all groups were ig for 7 d respectively. The neurobehavioral changes was studied with rota-rod treadmill test, after that, the brain of mice were detected by immunohistochemistry with labeling of Nestin and pathological observation at 7 days after BCAO. It was found that, proliferation of NSCs was increased by BMECG in in vitro and in vivo. And BMECG significantly improved the time of staying in the rota-rod, it can promote the foundction of in cerebral cortex. It is concluded that these results further support the hypothesis that neuroprotective effect of BMECG may relate to the ability of stimulating self-renew of NSCs, which can be provided a new insight and strategy of anti-neuropathy of stroke.


Assuntos
Animais , Humanos , Masculino , Camundongos , Ratos , Diferenciação Celular , Proliferação de Células , Células Cultivadas , Infarto Cerebral , Tratamento Farmacológico , Medicamentos de Ervas Chinesas , Farmacologia , Células-Tronco Neurais , Biologia Celular , Neurogênese , Neurônios , Biologia Celular , Fármacos Neuroprotetores , Farmacologia , Ratos Wistar
3.
Journal of International Pharmaceutical Research ; (6): 743-746, 2013.
Artigo em Chinês | WPRIM | ID: wpr-845856

RESUMO

JAK/STAT is a pleiotropic signal transduction pathway with functions of regulating proliferation, differentiation and apoptosis in the cell. Recent research has shown that it plays an important role in embryonic development, brain tumors, cerebral ischemia and neural stem cell(NSC) proliferation process after brain injuries. Notch signaling pathway exists in all known animal cells, and it is a classic signaling pathway in the regulation of NSC proliferation and differentiation. Under the guidance of the network pharmacology, this article casts light on the crosstalk between JAK/STAT and Notch signal pathway in NSC proliferation, with the aim to provide basic theoretical supports in the research of drugs with the effectiveness of neuroprotection and NSC regulation after cerebral ischemia.

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