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Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations

Parkinson’s disease (PD) is a progressive neuroinflammatory and degenerative disease. In this study, we investigated the neuroprotective action of betanin in the rotenone-induced Parkinson-like mice model. Twenty-eight adult male Swiss albino mice were divided into four groups: Vehicle, Rotenone, Ro...

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Published in:Biomedicine & pharmacotherapy 2023-08, Vol.164, p.114917-114917, Article 114917
Main Authors: ElSayed, Mohamed H., Atif, Huda M., Eladl, Mohamed Ahmed, Elaidy, Samah M., Helaly, Ahmed M.N., Hisham, Fatma Azzahraa, Farag, Noha E., Osman, Noura M.S., Ibrahiem, Afaf T., Khella, Heba W.Z., Bilasy, Shymaa E., Albalawi, Marzough Aziz, Helal, Mohamed A., Alzlaiq, Wafa Ali, Zaitone, Sawsan A.
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cited_by cdi_FETCH-LOGICAL-c3237-e18fac0a28c1bcb2ef549cd8d117f3978e97e486d6cb73a997cdea86d2cc273d3
cites cdi_FETCH-LOGICAL-c3237-e18fac0a28c1bcb2ef549cd8d117f3978e97e486d6cb73a997cdea86d2cc273d3
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container_title Biomedicine & pharmacotherapy
container_volume 164
creator ElSayed, Mohamed H.
Atif, Huda M.
Eladl, Mohamed Ahmed
Elaidy, Samah M.
Helaly, Ahmed M.N.
Hisham, Fatma Azzahraa
Farag, Noha E.
Osman, Noura M.S.
Ibrahiem, Afaf T.
Khella, Heba W.Z.
Bilasy, Shymaa E.
Albalawi, Marzough Aziz
Helal, Mohamed A.
Alzlaiq, Wafa Ali
Zaitone, Sawsan A.
description Parkinson’s disease (PD) is a progressive neuroinflammatory and degenerative disease. In this study, we investigated the neuroprotective action of betanin in the rotenone-induced Parkinson-like mice model. Twenty-eight adult male Swiss albino mice were divided into four groups: Vehicle, Rotenone, Rotenone + Betanin 50 mg/kg, and Rotenone + Betanin 100 mg/kg. Parkinsonism was induced by subcutaneous injection of 9 doses of rotenone (1 mg/kg/48 h) plus betanin at 50 and 100 mg/kg/48 h in rotenone + betanin groups for twenty days. Motor dysfunction was assessed after the end of the therapeutic period using the pole, rotarod, open-field, grid, and cylinder tests. Malondialdehyde, reduced glutathione (GSH), Toll-like receptor 4 (TLR4), myeloid differentiation primary response-88 (MyD88), nuclear factor kappa- B (NF-κB), neuronal degeneration in the striatum were evaluated. In addition, we assessed the immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in substantia nigra compacta (SNpc). Our results showed that rotenone remarkably decreased (results of tests), increased decreased TH density with a significant increase in MDA, TLR4, MyD88, NF-κB, and a decrease in GSH (p 
doi_str_mv 10.1016/j.biopha.2023.114917
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In this study, we investigated the neuroprotective action of betanin in the rotenone-induced Parkinson-like mice model. Twenty-eight adult male Swiss albino mice were divided into four groups: Vehicle, Rotenone, Rotenone + Betanin 50 mg/kg, and Rotenone + Betanin 100 mg/kg. Parkinsonism was induced by subcutaneous injection of 9 doses of rotenone (1 mg/kg/48 h) plus betanin at 50 and 100 mg/kg/48 h in rotenone + betanin groups for twenty days. Motor dysfunction was assessed after the end of the therapeutic period using the pole, rotarod, open-field, grid, and cylinder tests. Malondialdehyde, reduced glutathione (GSH), Toll-like receptor 4 (TLR4), myeloid differentiation primary response-88 (MyD88), nuclear factor kappa- B (NF-κB), neuronal degeneration in the striatum were evaluated. In addition, we assessed the immunohistochemical densities of tyrosine hydroxylase (TH) in Str and in substantia nigra compacta (SNpc). Our results showed that rotenone remarkably decreased (results of tests), increased decreased TH density with a significant increase in MDA, TLR4, MyD88, NF-κB, and a decrease in GSH (p &lt; 0.05). Treatment with betanin significantly results of tests), increased TH density. Furthermore, betanin significantly downregulated malondialdehyde and improved GSH. Additionally, the expression of TLR4, MyD88, and NF-κB was significantly alleviated. Betanin’s powerful antioxidative and anti-inflammatory properties can be related to its neuroprotective potential as well as its ability to delay or prevent neurodegeneration in PD.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2023.114917</identifier><identifier>PMID: 37244180</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>Animals ; Betacyanins - pharmacology ; Betanin ; Down-Regulation ; Experimental Parkinsonism ; Male ; Malondialdehyde ; Mice ; Molecular docking ; Molecular Docking Simulation ; Mouse ; Myeloid Differentiation Factor 88 - metabolism ; NF-kappa B - metabolism ; Parkinson Disease - drug therapy ; Parkinson Disease - metabolism ; Parkinsonian Disorders - chemically induced ; Parkinsonian Disorders - drug therapy ; Parkinsonian Disorders - metabolism ; Rotenone - adverse effects ; TLR4/MyD88/NF-κB pathway ; Toll-Like Receptor 4 - metabolism</subject><ispartof>Biomedicine &amp; pharmacotherapy, 2023-08, Vol.164, p.114917-114917, Article 114917</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. 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Our results showed that rotenone remarkably decreased (results of tests), increased decreased TH density with a significant increase in MDA, TLR4, MyD88, NF-κB, and a decrease in GSH (p &lt; 0.05). Treatment with betanin significantly results of tests), increased TH density. Furthermore, betanin significantly downregulated malondialdehyde and improved GSH. Additionally, the expression of TLR4, MyD88, and NF-κB was significantly alleviated. Betanin’s powerful antioxidative and anti-inflammatory properties can be related to its neuroprotective potential as well as its ability to delay or prevent neurodegeneration in PD.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>37244180</pmid><doi>10.1016/j.biopha.2023.114917</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record>
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subjects Animals
Betacyanins - pharmacology
Betanin
Down-Regulation
Experimental Parkinsonism
Male
Malondialdehyde
Mice
Molecular docking
Molecular Docking Simulation
Mouse
Myeloid Differentiation Factor 88 - metabolism
NF-kappa B - metabolism
Parkinson Disease - drug therapy
Parkinson Disease - metabolism
Parkinsonian Disorders - chemically induced
Parkinsonian Disorders - drug therapy
Parkinsonian Disorders - metabolism
Rotenone - adverse effects
TLR4/MyD88/NF-κB pathway
Toll-Like Receptor 4 - metabolism
title Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations
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