Angiotensin-(1-7) improves cognitive function in rats with chronic cerebral hypoperfusion.
Chronic cerebral hypoperfusion (CCH) is associated with cognitive decline in aging, vascular dementia and Alzheimer׳s disease. Recently, angiotensin-(1-7) (Ang-(1-7)), one of the physiological constituents of the brain, was found to protect against cognitive dysfunction and brain ischemia. However, the effects of Ang-(1-7) on CCH-induced cognitive deficits remained unknown. In the present study, Ang-(1-7) significantly alleviated CCH-induced cognitive deficits in rats subjected to permanent bilateral occlusion of the common carotid arteries (a model of CCH). This neuroprotective effect was associated with increased nitric oxide generation, attenuated neuronal loss and suppressed astrocyte proliferation in the hippocampus. These findings demonstrate that Ang-(1-7) is a promising therapeutic agent for CCH-induced cognitive deficits.
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China.
Wei
W
Xie
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China.
Donglin
D
Zhu
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China.
Li
L
Ji
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China.
Minjie
M
Tian
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China.
Chang
C
Xu
Department of Neurology, Nanjing Brain Hospital, Nanjing Medical University, P.O. Box 210029, No. 264 Guangzhou Road, Nanjing, PR China; Department of Neurology, School of Medicine, Nanjing University, P.O. Box 210093, No. 22 Hankou Road, Nanjing, PR China. Electronic address: profshijp@163.com.
Jingping
J
Shi
D000803:Angiotensin I / Q000494:pharmacology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology*; D017536:Carotid Artery, Common; D016923:Cell Death / Q000187:drug effects; D049109:Cell Proliferation / Q000187:drug effects; D002908:Chronic Disease; D003072:Cognition Disorders / Q000188:drug therapy* / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D004195:Disease Models, Animal; D006624:Hippocampus / Q000187:drug effects / Q000473:pathology / Q000503:physiopathology; D008297:Male; D018782:Maze Learning / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000473:pathology / Q000502:physiology; D018696:Neuroprotective Agents / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism; D010446:Peptide Fragments / Q000494:pharmacology*; D017208:Rats, Wistar
D018696:Neuroprotective Agents; D010446:Peptide Fragments; D009569:Nitric Oxide; D000803:Angiotensin I; C118790:angiotensin I (1-7)
Angiotensin-(1-7); Astrocyte proliferation; Chronic cerebral hypoperfusion; Hippocampus; Neuronal loss; Nitric oxide