ObjectiveTo investigate the effect of serum on the differentiation of neural stem cells.MethodsThe neural stem cells were isolated from the embryonic hippocampus tissues of Sprague Dawley rats at 14 day of pregnancy. After culturing and passaging, the 3rd generation cells were identified by immunocytochemical staining. Then, the cells were divided into 3 groups according to the concentrations of fetal bovine serum (FBS) used in the differentiation cell culture medium: 5% (group A), 1% (group B), 0 (group C), respectively. The other components of the culture media in 3 groups were the same. Cell viability was determined by using the Live/Dead cell staining at 8 days; the expressions of glial cell marker [glial fibrillary acidic protein (GFAP)] and neuronal marker (β-Ⅲ Tubulin) were determined and analyzed by immunocytochemical staining and real-time fluorescent PCR at 4 and 8 days of culture.ResultsBased on cell morphology and immunocytochemical staining, neural stem cells were identified. Cells were growing well with no death in all groups. With decreasing FBS concentration, the expression of GFAP was significantly decreased on both protein and mRNA level, whereas the expression of β-Ⅲ Tubulin was evidently increased. The staining of each group at 8 days was more obvious than that at 4 days. There were significant differences in mRNA expressions of GFAP and β-Ⅲ Tubulin at 4 and 8 days between groups (P<0.05).ConclusionSerum can promote the differentiation of neural stem cells into glial cells. At the same time, it inhibits the differentiation of neural stem cells into neurons, the lower the serum concentration, the smaller the effect.
ObjectiveTo summarize the current research progress on the changes of enteric glial cells (EGCs) in intestinal motility disorders and its possible molecular mechanisms in regulating intestinal motility.MethodThe literatures related to the EGCs and intestinal dysmotility were collected and analyzed.ResultsThe EGCs were involved in the occurrence and development of intestinal motility disorders, and there were abnormalities in the quantity, receptor, and phenotype in the different dysmotility diseases such as the postoperative ileus, Hirschsprung disease, inflammatory bowel disease, diabetes and so on. It could sense the neuronal signals and communicate with the enteric neurons via Ca2+ response and connexin-43 to affect the intestinal motility.ConclusionStudy of role and mechanism of EGCs in intestinal motor dysfunction is helpful to discovery new targets for treatment of these diseases.
Ischemic stroke (IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.