|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage显示文摘The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral ischemia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb1, an active component of ginseng, and cortical neurons. Ginsenoside Rb1 protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rb1 inhibited levels of tumor necrosis factor-α in a co-culture system containing activated N9 microglial cells. Ginsenoside Rb1 also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rb1 attenuates damage to cerebral cortex neurons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-α expression in hypoxia-activated microglia. | Lining Ke Wei Guo Jianwen Xu Guodong Zhang Wei Wang Wenhua Huang | 2014 | Neural Regeneration Research2014，9，3： | 11 |
| 2 | Multi- objective flexible job shop schedule: design and evalu- ation by simulation modeling显示文摘 | Xing Lining Chen Ying-wu Yang Ke wei | 2009 | Applied Soft Com- puting2009，9，： | 1 |
| 3 | S100P-binding protein,S100PBP,mediates adhesion through regulation of cathepsin Z in pancreatic cancer cells显示文摘 | Lines KE Chelala C Dmitrovic B | 2012 | Am J Pathol2012，180，4： | 1 |
| 4 | Electrophysiologic and phenotypic features of an autosomal cone-rod dystrophy caused by a novel CRX mutation显示文摘 | Lines MA Hébert M McTaggart KE | | 0，，： | 1 |
| 5 | Hovo safe are serotonin reaptake inhibitors depreission in patients with coronary heart disease显示文摘 | She line Y1 Freed land KE Carney RM | 1997 | Am Med1997，102，： | 1 |
| 6 | In situ direct reprogramming of astrocytes to neurons via polypyrimidine tract-binding protein 1 knockdown in a mouse model of ischemic stroke显示文摘In situ direct reprogramming technology can directly convert endogenous glial cells into functional neurons in vivo for central nervous system repair. Polypyrimidine tract-binding protein 1(PTB) knockdown has been shown to reprogram astrocytes to functional neurons in situ. In this study, we used AAV-PHP.e B-GFAP-sh PTB to knockdown PTB in a mouse model of ischemic stroke induced by endothelin-1, and investigated the effects of GFAP-sh PTB-mediated direct reprogramming to neurons. Our results showed that in the mouse model of ischemic stroke, PTB knockdown effectively reprogrammed GFAP-positive cells to neurons in ischemic foci, restored neural tissue structure, reduced inflammatory response, and improved behavioral function. These findings validate the effectiveness of in situ transdifferentiation of astrocytes, and suggest that the approach may be a promising strategy for stroke treatment. | Meng Yuan Yao Tang Tianwen Huang Lining Ke En Huang | 2024 | Neural Regeneration Research2024，19，10： | 0 |
您所在的机构暂未开通此部分的功能，请联系管理员