TGF-β1 Protection against Aβ1–42-Induced Neuroinflammation and Neurodegeneration in RatsReportar como inadecuado




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1

School of Biological & Basic Medical Sciences, Soochow University, 199 Renai Road, Suzhou 215123, China

2

Department of Physiology, School of Medicine, Nantong University, 19 Qixiu Road, Nantong 226001, China

3

Co-innovation Center of Neuroregeneration, Nantong University, 19 Qixiu Road, Nantong 226001, China





*

Authors to whom correspondence should be addressed.



Abstract Transforming growth factor TGF-β1, a cytokine that can be expressed in the brain, is a key regulator of the brain’s responses to injury and inflammation. Alzheimer’s disease AD, the most common neurodegenerative disorder, involves inflammatory processes in the brain in addition to the hallmarks, amyloid-β Aβ plaques and neurofibrillary tangles. Recently, we have shown that T-helper Th 17 cells, a subpopulation of CD4+ T-cells with high proinflammation, also participate in the brain inflammatory process of AD. However, it is poorly known whether TGF-β1 ameliorates the lymphocyte-mediated neuroinflammation and, thereby, alleviates neurodegeneration in AD. Herein, we administered TGF-β1 via the intracerebroventricle ICV in AD model rats, by Aβ1–42 injection in both sides of the hippocampus, to show the neuroprotection of TGF-β1. The TGF-β1 administration after the Aβ1–42 injection ameliorated cognitive deficit and neuronal loss and apoptosis, reduced amyloid precursor protein APP expression, elevated protein phosphatase PP2A expression, attenuated glial activation and alleviated the imbalance of the pro-inflammatory-anti-inflammatory responses of T-lymphocytes, compared to the Aβ1–42 injection alone. These findings demonstrate that TGF-β1 provides protection against AD neurodegeneration and suggest that the TGF-β1 neuroprotection is implemented by the alleviation of glial and T-cell-mediated neuroinflammation. View Full-Text

Keywords: TGF-β1; Alzheimer’s disease; Aβ1–42; T-lymphocytes; microglia TGF-β1; Alzheimer’s disease; Aβ1–42; T-lymphocytes; microglia





Autor: Wei-Xing Shen 1,2, Jia-Hui Chen 2, Jian-Hua Lu 2, Yu-Ping Peng 2,3,* and Yi-Hua Qiu 2,3,*

Fuente: http://mdpi.com/



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