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Cited by 90Parkinson's Disease Mechanisms and TreatmentsRenin-Angiotensin System StudiesNuclear Receptors and Signaling

Angiotensin 1–7 ameliorates 6-hydroxydopamine lesions in hemiparkinsonian rats through activation of MAS receptor/PI3K/Akt/BDNF pathway and inhibition of angiotensin II type-1 receptor/NF-κB axis

Rabie, Mostafa A., Abd El Fattah, Mai A., Nassar, Noha N., El-Abhar, Hanan S., Abdallah, Dalaal M.·2018·Biochemical Pharmacology
DOI 10.1016/j.bcp.2018.01.047
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Abstract

MAS receptor (MASR), expressed in several brain areas, conferred neuroprotection against neurodegenerative disorders when activated by angiotensin (Ang) 1-7; however, its role in Parkinson's disease (PD) remains elusive. Intra-striatal post-administration of Ang1-7, using a 6-hydroxydopamine (OHDA) PD model, improved motor performance and muscle coordination. On the molecular level, Ang1-7 upregulated the striatal expression of MASR and caused upsurge in its downstream targets (p-PI3K/p-Akt/p-CREB/BDNF) to phosphorylate TrKB, which in a positive feedback upregulates MASR. Moreover, Ang1-7 increased substantia nigral tyrosine hydroxylase (TH) expression and striatal dopamine (DA) content to indicate the preservation of the dopaminergic neuronal signal. This effect extended to inhibit the striatal expression of Ang II type-1 receptor (AT-1R) to hold the neurodegenerative effect and to boost Ang1-7 anti-inflammatory/antioxidant effects by abating NADPH oxidase, along with lipid peroxidation. Indeed, Ang1-7 was able to decrease p-MAPK p38/NF-κB p65 to level the inflammatory and oxidative stress events off. The Ang1-7-mediated activation of MASR cue and the suppression of the AT-1R cascade were partially reversed by the intrastartial injection of A-779, a MASR antagonist. The current data suggests a novel therapeutic potential for the Ang1-7 against neurotoxicity associated motor impairment related to PD. The anti-parkinsonian effect of Ang1-7, is in part, mediated by its binding to MASR and the initiation of PI3K/Akt/CREB/BDNF/TrKB cue to increase DA synthesis, besides the downregulation/inhibition of AT-1R/MAPK p38/NF-κB p65/NADPH oxidase pathway.

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  • Physical exercise causes activation of CREB by signal transducers such as MAPKs, CaMK, and NMDA-R in hippocampal and striatal plasticity.

    “Application of physical exercises causes activation of CREB by different signal transducers, such as MAPKs, CaMK, and N-methyl-D-aspartate receptor (NMDA-R) in both the hippocampal and striatal plasticity [195,196].”

    From BDNF as a Promising Therapeutic Agent in Parkinson’s Disease (2020) · cites this paper as [196]

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Authors
Rabie, M. A., Abd El Fattah, M. A., Nassar, N. N., El-Abhar, H. S., & Abdallah, D. M.
Affiliations
Cairo University (EG)
Corresponding author
El-Abhar, Hanan S.
ORCID
Venue
Biochemical Pharmacology
Publisher
Elsevier BV
Published
2018-05
Volume
151
Pages
126-134
ISSN
0006-2952 (ISSN-L)
DOI
10.1016/j.bcp.2018.01.047
OpenAlex
W2794280748
Cited by
90
References
68
Citations by year
2026: 10 · 2025: 12 · 2024: 15 · 2023: 10 · 2022: 14 · 2021: 14 · 2020: 9 · 2019: 6
FWCI
4.92
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Biochemical Pharmacology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
Keywords
angiotensin-(1-7), Mas receptor, Parkinson's disease, 6-hydroxydopamine lesion, neuroprotection, angiotensin II type 1 receptor, NF-κB, p38 MAPK, NADPH oxidase, oxidative stress, neuroinflammation, dopaminergic neurons, substantia nigra, striatum, motor impairment, A779
MeSH terms
Proto-Oncogene Mas, Angiotensin I, Animals, Behavior, Animal, Corpus Striatum, Male, Peptide Fragments, Proto-Oncogene Proteins, Signal Transduction, NF-kappa B, Oxidopamine, Rats, Wistar, Brain-Derived Neurotrophic Factor, Phosphatidylinositol 3-Kinases, Parkinsonian Disorders, Receptors, G-Protein-Coupled, Receptor, Angiotensin, Type 1, Proto-Oncogene Proteins c-akt

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