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Tytuł pozycji:

Vildagliptin Attenuates Huntington's Disease through Activation of GLP-1 Receptor/PI3K/Akt/BDNF Pathway in 3-Nitropropionic Acid Rat Model.

Tytuł:
Vildagliptin Attenuates Huntington's Disease through Activation of GLP-1 Receptor/PI3K/Akt/BDNF Pathway in 3-Nitropropionic Acid Rat Model.
Autorzy:
Sayed NH; Department of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Fathy N; Department of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt. .
Kortam MA; Department of Biochemistry, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Rabie MA; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Mohamed AF; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Kamel AS; Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Governorate, Giza, Egypt.
Źródło:
Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics [Neurotherapeutics] 2020 Jan; Vol. 17 (1), pp. 252-268.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Publication: 2024- : [New York] : Elsevier Inc. on behalf of American Society for Experimental NeuroTherapeutics
Original Publication: Orlando, FL : Elsevier, c2007-
MeSH Terms:
Corpus Striatum/*drug effects
Corpus Striatum/*metabolism
Dipeptidyl-Peptidase IV Inhibitors/*administration & dosage
Huntington Disease/*metabolism
Signal Transduction/*drug effects
Vildagliptin/*administration & dosage
Animals ; Behavior, Animal/drug effects ; Brain-Derived Neurotrophic Factor/metabolism ; Corpus Striatum/pathology ; Disease Models, Animal ; Glucagon-Like Peptide-1 Receptor/metabolism ; Huntington Disease/chemically induced ; Male ; Maze Learning/drug effects ; Nitro Compounds/administration & dosage ; Phosphatidylinositol 3-Kinase/metabolism ; Propionates/administration & dosage ; Proto-Oncogene Proteins c-akt/metabolism ; Rats, Wistar ; Rotarod Performance Test
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Contributed Indexing:
Keywords: 3-nitropropionic acid; Glucagon like peptide-1; Mitochondrial dysfunction; PI3K/Akt signaling; Vildagliptin
Substance Nomenclature:
0 (Bdnf protein, rat)
0 (Brain-Derived Neurotrophic Factor)
0 (Dipeptidyl-Peptidase IV Inhibitors)
0 (Glp1r protein, rat)
0 (Glucagon-Like Peptide-1 Receptor)
0 (Nitro Compounds)
0 (Propionates)
EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
I6B4B2U96P (Vildagliptin)
QY4L0FOX0D (3-nitropropionic acid)
Entry Date(s):
Date Created: 20191116 Date Completed: 20210204 Latest Revision: 20240204
Update Code:
20240205
PubMed Central ID:
PMC7007456
DOI:
10.1007/s13311-019-00805-5
PMID:
31728850
Czasopismo naukowe
Vildagliptin (Vilda), a dipeptidyl peptidase-4 (DPP-4) inhibitor, has been highlighted as a promising therapeutic agent for neurodegenerative diseases as Alzheimer's and Parkinson's diseases. Vilda's effect is mostly linked to PI3K/Akt signaling in CNS. Moreover, PI3K/Akt activation reportedly enhanced survival and dampened progression of Huntington's disease (HD). However, Vilda's role in HD is yet to be elucidated. Thus, the aim of the study is to uncover the potentiality of Vilda in HD and unfold its link with PI3K/Akt pathway in 3-nitropropionic acid (3NP) rat model. Rats were randomly assigned into 4 groups; group 1 received saline, whereas, groups 2, 3 and 4 received 3NP (10 mg/kg/day; i.p.) for 14 days, concomitantly with Vilda (5 mg/kg/day; p.o.) in groups 3 and 4, and wortmannin (WM), a PI3K inhibitor, (15 μg/kg/day; i.v.) in group 4. Vilda improved cognitive and motor perturbations induced by 3NP, as confirmed by striatal histopathological specimens and immunohistochemical examination of GFAP. The molecular signaling of Vilda was estimated by elevation of GLP-1 level and protein expressions of survival proteins; p85/p55 (pY458/199)-PI3K, pS473-Akt. Together, it boosted striatal neurotrophic factors and receptor; pS133-CREB, BDNF, pY515-TrKB, which subsequently maintained mitochondrial integrity, as indicated by enhancing both SDH and COX activities, and the redox modulators; Sirt1, Nrf2. Such neuroprotection restored imbalance of neurotransmitters through increasing GABA and suppressing glutamate as well PDE10A. These effects were reversed by WM pre-administration. In conclusion, Vilda purveyed significant anti-Huntington effect which may be mediated, at least in part, via activation of GLP-1/PI3K/Akt pathway in 3NP rat model.
Erratum in: Neurotherapeutics. 2022 Mar;19(2):686. (PMID: 35352287)

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