Research Paper Volume 10, Issue 4 pp 645—657
AVE0991, a nonpeptide analogue of Ang-(1-7), attenuates aging-related neuroinflammation
- 1 Department of Neurology, Nanjing First Hospital Nanjing Medical University, Nanjing, PR China
- 2 Department of Neurology, Huai'an First People's Hospital, Nanjing Medical University, Huai'an, PR China
received: February 9, 2018 ; accepted: April 14, 2018 ; published: April 17, 2018 ;https://doi.org/10.18632/aging.101419
How to Cite
Copyright: Jiang et al. This is an open‐access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
During the aging process, chronic neuroinflammation induced by microglia is detrimental for the brain and contributes to the etiology of several aging-related neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. As a newly identified axis of renin-angiotensin system, ACE2/Ang-(1-7)/MAS1 axis plays a crucial role in modulating inflammatory responses under various pathological conditions. However, its relationship with aging-related neuroinflammation is less studied so far. In this study, by using SAMP8 mice, an animal model of accelerated aging, we revealed that the neuroinflammation in the aged brain might be attributed to a decreased level of Ang-(1-7). More importantly, we provided evidence that AVE0991, a nonpeptide analogue of Ang-(1-7), attenuated the aging-related neuroinflammation via suppression of microglial-mediated inflammatory response through a MAS1 receptor-dependent manner. Meanwhile, this protective effect might be ascribed to the M2 activation of microglia induced by AVE0991. Taken together, these findings reveal the association of Ang-(1-7) with the inflammatory response in the aged brain and uncover the potential of its nonpeptide analogue AVE0991 in attenuation of aging-related neuroinflammation.