Journal
JOURNAL OF THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM
Volume 19, Issue 3, Pages -Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/1470320318799587
Keywords
Angiotensin IV; chronic cerebral hypoperfusion; inflammation; vascular dementia; Alzheimer's disease
Categories
Funding
- National Natural Science Foundation of China [81771140]
- Natural Science Foundation of Jiangsu Province [BK20151084]
- Key Research and Development Project of Jiangsu Province [BL2014014]
- Six Talent Summit Foundation of Jiangsu Province [2016-WSN-180]
- Youth Medical Talent Program of Jiangsu Province [QNRC2016068]
- Medical Innovation Team of Jiangsu Province [CXTDA2017030]
- Nanjing Medical Science and Technology Development Foundation for Distinguished Young Scholars [JQX17008]
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Introduction: This study aimed to evaluate the influence of central angiotensin IV (Ang IV) infusion on chronic cerebral hypoperfusion (CCH)-related neuropathological changes including amyloid- (A), hyperphosphorylated tau (p-tau) and the inflammatory response. Materials and methods: Rats with CCH received central infusion of Ang IV, its receptor AT(4)R antagonist divalinal-Ang IV or artificial cerebrospinal fluid for six weeks. During this procedure, the systolic blood pressure (SBP) was monitored, and the levels of A(42), p-tau and pro-inflammatory cytokines in the brain were detected. Results: Rats with CCH exhibited higher levels of A(42), p-tau and pro-inflammatory cytokines in the brain when compared with controls. Infusion of Ang IV significantly reduced the expression of pro-inflammatory cytokines in the brains of rats with CCH. Meanwhile, the reduction of pro-inflammatory cytokines levels caused by Ang IV was reversed by divalinal-Ang IV. During the treatment, the SBP in rats was not significantly altered. Conclusion: This study demonstrates for the first time that Ang IV dose-dependently suppresses inflammation through AT(4)R in the brains of rats with CCH, which is independent from SBP. These findings suggest that Ang IV/AT(4)R may represent a potential therapeutic target for CCH-related neurological diseases.
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