PubMed | Wuxi Childrens Hospital Wuxi 214000
Type: Journal Article | Journal: International journal of clinical and experimental medicine | Year: 2015
More and more evidences suggestted that ApoE plays an important role in modulating the systemic and central nervous inflammatory responses. However, there is a lack of exacted mechanism of ApoE. In this study, we aimed to investigate whether apolipoprotein E (ApoE) induced inflammatory responses and apoptosis in neonatal mice brain from ApoE deficient (ApoE(-/-)) and wildtype (WT). Compared to control group, the microglia cell from ApoE(-/-) mice showed more severe inflammation and cell death such as iNOS and IL-1. Furthermore, anti-inflammatory such as TGF-, IL-10 from microglia and astrocytes in ApoE(-/-) mice were decreased. On the other way, TGF- from astrocytes can inhibit inflammation factors secretion from microglia. Our findings suggested that the anti- inflammation factor such as IL-10 mainly from microglia and TGF- mainly from astrocyte is significant decreased after Loss of ApoE function in ApoE(-/-) mice which induced severe inflammation. Furthrtmore, anti- inflammation factor such as IL-10 and TGF- Therefore, we conclude that apolipoprotein E knockout induced inflammatory responses related to microglia in neonatal mice brain via astrocytes.