原创力文档vip enhances phagocytosis of fibrillar beta-amyloid by microglia and attenuates amyloid deposition in the brain of appps1 micevip增强吞噬小胶质细胞和纤维β-淀粉样蛋白的变弱appps1老鼠大脑中的淀粉样蛋白沉积.pdfVIP
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vip enhances phagocytosis of fibrillar beta-amyloid by microglia and attenuates amyloid deposition in the brain of appps1 micevip增强吞噬小胶质细胞和纤维β-淀粉样蛋白的变弱appps1老鼠大脑中的淀粉样蛋白沉积
VIP Enhances Phagocytosis of Fibrillar Beta-Amyloid by
Microglia and Attenuates Amyloid Deposition in the
Brain of APP/PS1 Mice
1. 2. 1 1 1 1
Min Song , Jia-xiang Xiong , Yan-yan Wang , Jun Tang , Bo Zhang , Yun Bai *
1 Department of Medical Genetics, Third Military Medical University, ChongQing, China, 2 Department of Medical Physiology,Third Military Medical University, ChongQing,
China
Abstract
Vasoactive intestinal peptide (VIP) is a multifunctional neuropeptide with demonstrated immunosuppressive and
neuroprotective activities. It has been shown to inhibit Amyloid beta (Ab)-induced neurodegeneration by indirectly
suppressing the production and release of a variety of inflammatory and neurotoxic factors by activated microglia. We
demonstrated that VIP markedly increased microglial phagocytosis of fibrillar Ab42 and that this enhanced phagocytotic
activity depended on activation of the Protein kinase C (PKC) signaling pathway. In addition, VIP suppressed the release of
tumor necrosis factor alpha (TNF-a) and nitric oxide(NO) from microglia activated by combined treatment with fibrillar Ab42
and low dose interferon-c (IFN-c). We utilized an adenovirus-mediated gene delivery method to overexpress VIP
constitutively in the hippocampus of APPswPS1 transgenic mice. The Ab load was significantly reduced in the hippocampus
of this animal model of Alzheimer’s disease, possibly due to the accumulation and activation of cd11b-immunoactive
microglial cells. The modulation of microglial activation, phagocytosis, and secretion by VIP is a promising therapeutic
option for the treatment of Alzheimer’s disease(
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