Carbosilane dendrimers inhibit α-synuclein fibrillation and prevent cells from rotenone-induced damage

[Display omitted] This study investigates the role of carbosilane dendrimers in fibrillation of α-synuclein and prevention of the mouse hippocampal cell (mHippoE-18) from rotenone-induced damage. Examining the interaction between carbosilane dendrimers and α-synuclein, we found that the dendrimers i...

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Veröffentlicht in:International journal of pharmaceutics 2015-04, Vol.484 (1-2), p.268-275
Hauptverfasser: Milowska, Katarzyna, Szwed, Aleksandra, Mutrynowska, Marta, Gomez-Ramirez, Rafael, de la Mata, Francisco Javier, Gabryelak, Teresa, Bryszewska, Maria
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container_end_page 275
container_issue 1-2
container_start_page 268
container_title International journal of pharmaceutics
container_volume 484
creator Milowska, Katarzyna
Szwed, Aleksandra
Mutrynowska, Marta
Gomez-Ramirez, Rafael
de la Mata, Francisco Javier
Gabryelak, Teresa
Bryszewska, Maria
description [Display omitted] This study investigates the role of carbosilane dendrimers in fibrillation of α-synuclein and prevention of the mouse hippocampal cell (mHippoE-18) from rotenone-induced damage. Examining the interaction between carbosilane dendrimers and α-synuclein, we found that the dendrimers inhibit fibril formation. We also investigated cell viability, the production of reactive oxygen species (ROS), and mitochondrial membrane potential. mHippoE-18 cells were preincubated with carbosilane dendrimers before rotenone was added. All the dendrimers possess potential protection activity. Preincubation with dendrimers contributed to: increased viability, higher mitochondrial membrane potential, and reduced ROS level in cells. The probable mechanism of cell protection lies in the ability of dendrimers to capture rotenone by encapsulating or binding to its surface groups. The fact that dendrimers have prevention potential is important in the search for new pharmacological strategies against neurodegenerative disorders.
doi_str_mv 10.1016/j.ijpharm.2015.02.066
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All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-a9c80283a3eb787df32e41a189b115df7739271e791326722b617d47791a63bf3</citedby><cites>FETCH-LOGICAL-c365t-a9c80283a3eb787df32e41a189b115df7739271e791326722b617d47791a63bf3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ijpharm.2015.02.066$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25735664$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Milowska, Katarzyna</creatorcontrib><creatorcontrib>Szwed, Aleksandra</creatorcontrib><creatorcontrib>Mutrynowska, Marta</creatorcontrib><creatorcontrib>Gomez-Ramirez, Rafael</creatorcontrib><creatorcontrib>de la Mata, Francisco Javier</creatorcontrib><creatorcontrib>Gabryelak, Teresa</creatorcontrib><creatorcontrib>Bryszewska, Maria</creatorcontrib><title>Carbosilane dendrimers inhibit α-synuclein fibrillation and prevent cells from rotenone-induced damage</title><title>International journal of pharmaceutics</title><addtitle>Int J Pharm</addtitle><description>[Display omitted] This study investigates the role of carbosilane dendrimers in fibrillation of α-synuclein and prevention of the mouse hippocampal cell (mHippoE-18) from rotenone-induced damage. 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subjects alpha-Synuclein - antagonists & inhibitors
alpha-Synuclein - metabolism
Animals
Carbosilane dendrimers
Cell Line
Cell Survival - drug effects
Cell Survival - physiology
Dendrimers - pharmacology
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
Mice
Parkinson’s disease
Reactive Oxygen Species - metabolism
Rotenone
Rotenone - toxicity
Silanes - pharmacology
α-Synuclein
title Carbosilane dendrimers inhibit α-synuclein fibrillation and prevent cells from rotenone-induced damage
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