Beneficial effects of β-escin on muscle regeneration in rat model of skeletal muscle injury
•β-escin facilitates muscle regeneration.•β-escin rescues muscles from atrophy, reduces inflammation and decreases fibrosis.•β-escin reduces macrophage infiltration and promotes their M2 polarization.•β-escin alters transcription of muscle regeneration-related genes.•β-escin reduces secretion of MMP...
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Veröffentlicht in: | Phytomedicine (Stuttgart) 2021-12, Vol.93, p.153791-153791, Article 153791 |
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creator | Sikorska, Maria Dutkiewicz, Małgorzata Zegrocka – Stendel, Oliwia Kowalewska, Magdalena Grabowska, Iwona Koziak, Katarzyna |
description | •β-escin facilitates muscle regeneration.•β-escin rescues muscles from atrophy, reduces inflammation and decreases fibrosis.•β-escin reduces macrophage infiltration and promotes their M2 polarization.•β-escin alters transcription of muscle regeneration-related genes.•β-escin reduces secretion of MMP-9 and increases ALDH activity.
Recent advancements in understanding β-escin action provide basis for new therapeutic claims for the drug. β-escin-evoked attenuation of NF-κB-dependent signaling, increase in MMP-14 and decrease in COUP-TFII content and a rise in cholesterol biosynthesis could be beneficial in alleviating muscle-damaging processes.
The aim of this study was to investigate the effect of β-escin on skeletal muscle regeneration.
Rat model of cardiotoxin-induced injury of fast-twich extensor digitorum longus (EDL) and slow-twich soleus (SOL) muscles and C2C12 myoblast cells were used in the study. We evaluated muscles obtained on day 3 and 14 post-injury by histological analyses of muscle fibers, connective tissue, and mononuclear infiltrate, by immunolocalization of macrophages and by qPCR to quantify the expression of muscle regeneration-related genes. Mechanism of drug action was investigated in vitro by assessing cell viability, NF-κB activation, MMP-2 and MMP-9 secretion, and ALDH activity.
In rat model, β-escin rescues regenerating muscles from atrophy. The drug reduces inflammatory infiltration, increases the number of muscle fibers and decreases fibrosis. β-escin reduces macrophage infiltration into injured muscles and promotes their M2 polarization. It also alters transcription of muscle regeneration-related genes: Myf5, Myh2, Myh3, Myh8, Myod1, Pax3 and Pax7, and Pcna. In C2C12 myoblasts in vitro, β-escin inhibits TNF-α-induced activation of NF-κB, reduces secretion of MMP-9 and increases ALDH activity.
The data reveal beneficial role of β-escin in muscle regeneration, particularly in poorly regenerating slow-twitch muscles. The findings provide rationale for further studies on β-escin repositioning into conditions associated with muscle damage such as strenuous exercise, drug-induced myotoxicity or age-related disuse atrophy.
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doi_str_mv | 10.1016/j.phymed.2021.153791 |
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Recent advancements in understanding β-escin action provide basis for new therapeutic claims for the drug. β-escin-evoked attenuation of NF-κB-dependent signaling, increase in MMP-14 and decrease in COUP-TFII content and a rise in cholesterol biosynthesis could be beneficial in alleviating muscle-damaging processes.
The aim of this study was to investigate the effect of β-escin on skeletal muscle regeneration.
Rat model of cardiotoxin-induced injury of fast-twich extensor digitorum longus (EDL) and slow-twich soleus (SOL) muscles and C2C12 myoblast cells were used in the study. We evaluated muscles obtained on day 3 and 14 post-injury by histological analyses of muscle fibers, connective tissue, and mononuclear infiltrate, by immunolocalization of macrophages and by qPCR to quantify the expression of muscle regeneration-related genes. Mechanism of drug action was investigated in vitro by assessing cell viability, NF-κB activation, MMP-2 and MMP-9 secretion, and ALDH activity.
In rat model, β-escin rescues regenerating muscles from atrophy. The drug reduces inflammatory infiltration, increases the number of muscle fibers and decreases fibrosis. β-escin reduces macrophage infiltration into injured muscles and promotes their M2 polarization. It also alters transcription of muscle regeneration-related genes: Myf5, Myh2, Myh3, Myh8, Myod1, Pax3 and Pax7, and Pcna. In C2C12 myoblasts in vitro, β-escin inhibits TNF-α-induced activation of NF-κB, reduces secretion of MMP-9 and increases ALDH activity.
The data reveal beneficial role of β-escin in muscle regeneration, particularly in poorly regenerating slow-twitch muscles. The findings provide rationale for further studies on β-escin repositioning into conditions associated with muscle damage such as strenuous exercise, drug-induced myotoxicity or age-related disuse atrophy.
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Recent advancements in understanding β-escin action provide basis for new therapeutic claims for the drug. β-escin-evoked attenuation of NF-κB-dependent signaling, increase in MMP-14 and decrease in COUP-TFII content and a rise in cholesterol biosynthesis could be beneficial in alleviating muscle-damaging processes.
The aim of this study was to investigate the effect of β-escin on skeletal muscle regeneration.
Rat model of cardiotoxin-induced injury of fast-twich extensor digitorum longus (EDL) and slow-twich soleus (SOL) muscles and C2C12 myoblast cells were used in the study. We evaluated muscles obtained on day 3 and 14 post-injury by histological analyses of muscle fibers, connective tissue, and mononuclear infiltrate, by immunolocalization of macrophages and by qPCR to quantify the expression of muscle regeneration-related genes. Mechanism of drug action was investigated in vitro by assessing cell viability, NF-κB activation, MMP-2 and MMP-9 secretion, and ALDH activity.
In rat model, β-escin rescues regenerating muscles from atrophy. The drug reduces inflammatory infiltration, increases the number of muscle fibers and decreases fibrosis. β-escin reduces macrophage infiltration into injured muscles and promotes their M2 polarization. It also alters transcription of muscle regeneration-related genes: Myf5, Myh2, Myh3, Myh8, Myod1, Pax3 and Pax7, and Pcna. In C2C12 myoblasts in vitro, β-escin inhibits TNF-α-induced activation of NF-κB, reduces secretion of MMP-9 and increases ALDH activity.
The data reveal beneficial role of β-escin in muscle regeneration, particularly in poorly regenerating slow-twitch muscles. The findings provide rationale for further studies on β-escin repositioning into conditions associated with muscle damage such as strenuous exercise, drug-induced myotoxicity or age-related disuse atrophy.
[Display omitted]</description><subject>ALDH</subject><subject>macrophage</subject><subject>MMP, muscle</subject><subject>NF-κB</subject><subject>β-escin</subject><issn>0944-7113</issn><issn>1618-095X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp9kMtKxDAUhoMoOI6-gYsu3bTmtGnabAQdvMGAGwUXQmiTE03tZUxaYV7LB_GZzNBZSxYJ53z_D_kIOQeaAAV-2SSbj22HOklpCgnkWSHggCyAQxlTkb8ekgUVjMUFQHZMTrxvKAUmCrogbzfYo7HKVm2ExqAafTSY6PcnRq9sHw191E1etRg5fA-oq0YbZmETXlE3aGx3vP_EFsfQsYdt30xue0qOTNV6PNvfS_Jyd_u8eojXT_ePq-t1rLIyH-NaFJqCQVEBZymvMRxacKpYVlRQQF1kTGOZY204sNqYUgmqFePcaJ7qLFuSi7l344avCf0oO-sVtm3V4zB5meYlo5BDKQLKZlS5wXuHRm6c7Sq3lUDlTqZs5CxT7mTKWWaIXc0xDN_4tuhksIO9Qm1dcCb1YP8v-APsmoE9</recordid><startdate>202112</startdate><enddate>202112</enddate><creator>Sikorska, Maria</creator><creator>Dutkiewicz, Małgorzata</creator><creator>Zegrocka – Stendel, Oliwia</creator><creator>Kowalewska, Magdalena</creator><creator>Grabowska, Iwona</creator><creator>Koziak, Katarzyna</creator><general>Elsevier GmbH</general><scope>6I.</scope><scope>AAFTH</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>202112</creationdate><title>Beneficial effects of β-escin on muscle regeneration in rat model of skeletal muscle injury</title><author>Sikorska, Maria ; Dutkiewicz, Małgorzata ; Zegrocka – Stendel, Oliwia ; Kowalewska, Magdalena ; Grabowska, Iwona ; Koziak, Katarzyna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-b97d01fe9a16426bebeb0760c437a171b734de85ebf614bff8c90dc466fd62d33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>ALDH</topic><topic>macrophage</topic><topic>MMP, muscle</topic><topic>NF-κB</topic><topic>β-escin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sikorska, Maria</creatorcontrib><creatorcontrib>Dutkiewicz, Małgorzata</creatorcontrib><creatorcontrib>Zegrocka – Stendel, Oliwia</creatorcontrib><creatorcontrib>Kowalewska, Magdalena</creatorcontrib><creatorcontrib>Grabowska, Iwona</creatorcontrib><creatorcontrib>Koziak, Katarzyna</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Phytomedicine (Stuttgart)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sikorska, Maria</au><au>Dutkiewicz, Małgorzata</au><au>Zegrocka – Stendel, Oliwia</au><au>Kowalewska, Magdalena</au><au>Grabowska, Iwona</au><au>Koziak, Katarzyna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Beneficial effects of β-escin on muscle regeneration in rat model of skeletal muscle injury</atitle><jtitle>Phytomedicine (Stuttgart)</jtitle><date>2021-12</date><risdate>2021</risdate><volume>93</volume><spage>153791</spage><epage>153791</epage><pages>153791-153791</pages><artnum>153791</artnum><issn>0944-7113</issn><eissn>1618-095X</eissn><abstract>•β-escin facilitates muscle regeneration.•β-escin rescues muscles from atrophy, reduces inflammation and decreases fibrosis.•β-escin reduces macrophage infiltration and promotes their M2 polarization.•β-escin alters transcription of muscle regeneration-related genes.•β-escin reduces secretion of MMP-9 and increases ALDH activity.
Recent advancements in understanding β-escin action provide basis for new therapeutic claims for the drug. β-escin-evoked attenuation of NF-κB-dependent signaling, increase in MMP-14 and decrease in COUP-TFII content and a rise in cholesterol biosynthesis could be beneficial in alleviating muscle-damaging processes.
The aim of this study was to investigate the effect of β-escin on skeletal muscle regeneration.
Rat model of cardiotoxin-induced injury of fast-twich extensor digitorum longus (EDL) and slow-twich soleus (SOL) muscles and C2C12 myoblast cells were used in the study. We evaluated muscles obtained on day 3 and 14 post-injury by histological analyses of muscle fibers, connective tissue, and mononuclear infiltrate, by immunolocalization of macrophages and by qPCR to quantify the expression of muscle regeneration-related genes. Mechanism of drug action was investigated in vitro by assessing cell viability, NF-κB activation, MMP-2 and MMP-9 secretion, and ALDH activity.
In rat model, β-escin rescues regenerating muscles from atrophy. The drug reduces inflammatory infiltration, increases the number of muscle fibers and decreases fibrosis. β-escin reduces macrophage infiltration into injured muscles and promotes their M2 polarization. It also alters transcription of muscle regeneration-related genes: Myf5, Myh2, Myh3, Myh8, Myod1, Pax3 and Pax7, and Pcna. In C2C12 myoblasts in vitro, β-escin inhibits TNF-α-induced activation of NF-κB, reduces secretion of MMP-9 and increases ALDH activity.
The data reveal beneficial role of β-escin in muscle regeneration, particularly in poorly regenerating slow-twitch muscles. The findings provide rationale for further studies on β-escin repositioning into conditions associated with muscle damage such as strenuous exercise, drug-induced myotoxicity or age-related disuse atrophy.
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subjects | ALDH macrophage MMP, muscle NF-κB β-escin |
title | Beneficial effects of β-escin on muscle regeneration in rat model of skeletal muscle injury |
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