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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 |
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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 < 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 & pharmacotherapy, 2023-08, Vol.164, p.114917-114917, Article 114917</ispartof><rights>2023 The Authors</rights><rights>Copyright © 2023 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3237-e18fac0a28c1bcb2ef549cd8d117f3978e97e486d6cb73a997cdea86d2cc273d3</citedby><cites>FETCH-LOGICAL-c3237-e18fac0a28c1bcb2ef549cd8d117f3978e97e486d6cb73a997cdea86d2cc273d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37244180$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>ElSayed, Mohamed H.</creatorcontrib><creatorcontrib>Atif, Huda M.</creatorcontrib><creatorcontrib>Eladl, Mohamed Ahmed</creatorcontrib><creatorcontrib>Elaidy, Samah M.</creatorcontrib><creatorcontrib>Helaly, Ahmed M.N.</creatorcontrib><creatorcontrib>Hisham, Fatma Azzahraa</creatorcontrib><creatorcontrib>Farag, Noha E.</creatorcontrib><creatorcontrib>Osman, Noura M.S.</creatorcontrib><creatorcontrib>Ibrahiem, Afaf T.</creatorcontrib><creatorcontrib>Khella, Heba W.Z.</creatorcontrib><creatorcontrib>Bilasy, Shymaa E.</creatorcontrib><creatorcontrib>Albalawi, Marzough Aziz</creatorcontrib><creatorcontrib>Helal, Mohamed A.</creatorcontrib><creatorcontrib>Alzlaiq, Wafa Ali</creatorcontrib><creatorcontrib>Zaitone, Sawsan A.</creatorcontrib><title>Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><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 < 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><subject>Animals</subject><subject>Betacyanins - pharmacology</subject><subject>Betanin</subject><subject>Down-Regulation</subject><subject>Experimental Parkinsonism</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Mice</subject><subject>Molecular docking</subject><subject>Molecular Docking Simulation</subject><subject>Mouse</subject><subject>Myeloid Differentiation Factor 88 - metabolism</subject><subject>NF-kappa B - metabolism</subject><subject>Parkinson Disease - drug therapy</subject><subject>Parkinson Disease - metabolism</subject><subject>Parkinsonian Disorders - chemically induced</subject><subject>Parkinsonian Disorders - drug therapy</subject><subject>Parkinsonian Disorders - metabolism</subject><subject>Rotenone - adverse effects</subject><subject>TLR4/MyD88/NF-κB pathway</subject><subject>Toll-Like Receptor 4 - metabolism</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><recordid>eNp9kc1u1DAUhS0EokPhDRDykk1m_JOJHRZItFBAmgJCZW059s3UQ2KndjJlHolX4CF4JtxJYcnKuvJ3zv05CD2nZEkJrVa7ZePCcK2XjDC-pLSsqXiAFrRek6IiRDxECyLWvOCcsRP0JKUdIWRdcfkYnXDBypJKskA_z2DU3nns-iGGPSTchzFE3E7ejC54rL3Fuutg7_SYf-HHANH14Efd4S86fnc-Be9SjzOAbbj1EbZTp4_a0OKrzddydXl4K-Xq00Xx-9cZHvR4fasPr_Bl6MBkNGaZyT7bY6-8VBe2zmR75_M8o9sezdJT9KjVXYJn9-8p-nbx7ur8Q7H5_P7j-ZtNYTjjogAqW22IZtLQxjQM2nVZGystpaLltZBQCyhlZSvTCK7rWhgLOtfMGCa45afo5eyb73Ez5QFU75KBrtMewpQUk4wQJkvKMlrOqIkhpQitGvJtdDwoStRdSGqn5pDUXUhqDinLXtx3mJoe7D_R31Qy8HoGIO-5dxBVMg68AesimFHZ4P7f4Q8DL6m9</recordid><startdate>202308</startdate><enddate>202308</enddate><creator>ElSayed, Mohamed H.</creator><creator>Atif, Huda M.</creator><creator>Eladl, Mohamed Ahmed</creator><creator>Elaidy, Samah M.</creator><creator>Helaly, Ahmed M.N.</creator><creator>Hisham, Fatma Azzahraa</creator><creator>Farag, Noha E.</creator><creator>Osman, Noura M.S.</creator><creator>Ibrahiem, Afaf T.</creator><creator>Khella, Heba W.Z.</creator><creator>Bilasy, Shymaa E.</creator><creator>Albalawi, Marzough Aziz</creator><creator>Helal, Mohamed A.</creator><creator>Alzlaiq, Wafa Ali</creator><creator>Zaitone, Sawsan A.</creator><general>Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202308</creationdate><title>Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations</title><author>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.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3237-e18fac0a28c1bcb2ef549cd8d117f3978e97e486d6cb73a997cdea86d2cc273d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Betacyanins - pharmacology</topic><topic>Betanin</topic><topic>Down-Regulation</topic><topic>Experimental Parkinsonism</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Mice</topic><topic>Molecular docking</topic><topic>Molecular Docking Simulation</topic><topic>Mouse</topic><topic>Myeloid Differentiation Factor 88 - metabolism</topic><topic>NF-kappa B - metabolism</topic><topic>Parkinson Disease - drug therapy</topic><topic>Parkinson Disease - metabolism</topic><topic>Parkinsonian Disorders - chemically induced</topic><topic>Parkinsonian Disorders - drug therapy</topic><topic>Parkinsonian Disorders - metabolism</topic><topic>Rotenone - adverse effects</topic><topic>TLR4/MyD88/NF-κB pathway</topic><topic>Toll-Like Receptor 4 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>ElSayed, Mohamed H.</creatorcontrib><creatorcontrib>Atif, Huda M.</creatorcontrib><creatorcontrib>Eladl, Mohamed Ahmed</creatorcontrib><creatorcontrib>Elaidy, Samah M.</creatorcontrib><creatorcontrib>Helaly, Ahmed M.N.</creatorcontrib><creatorcontrib>Hisham, Fatma Azzahraa</creatorcontrib><creatorcontrib>Farag, Noha E.</creatorcontrib><creatorcontrib>Osman, Noura M.S.</creatorcontrib><creatorcontrib>Ibrahiem, Afaf T.</creatorcontrib><creatorcontrib>Khella, Heba W.Z.</creatorcontrib><creatorcontrib>Bilasy, Shymaa E.</creatorcontrib><creatorcontrib>Albalawi, Marzough Aziz</creatorcontrib><creatorcontrib>Helal, Mohamed A.</creatorcontrib><creatorcontrib>Alzlaiq, Wafa Ali</creatorcontrib><creatorcontrib>Zaitone, Sawsan A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>ElSayed, Mohamed H.</au><au>Atif, Huda M.</au><au>Eladl, Mohamed Ahmed</au><au>Elaidy, Samah M.</au><au>Helaly, Ahmed M.N.</au><au>Hisham, Fatma Azzahraa</au><au>Farag, Noha E.</au><au>Osman, Noura M.S.</au><au>Ibrahiem, Afaf T.</au><au>Khella, Heba W.Z.</au><au>Bilasy, Shymaa E.</au><au>Albalawi, Marzough Aziz</au><au>Helal, Mohamed A.</au><au>Alzlaiq, Wafa Ali</au><au>Zaitone, Sawsan A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Betanin improves motor function and alleviates experimental Parkinsonism via downregulation of TLR4/MyD88/NF-κB pathway: Molecular docking and biological investigations</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2023-08</date><risdate>2023</risdate><volume>164</volume><spage>114917</spage><epage>114917</epage><pages>114917-114917</pages><artnum>114917</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>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 < 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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