Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes
Identifieur interne : 000082 ( Pmc/Checkpoint ); précédent : 000081; suivant : 000083Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes
Auteurs : Shou-Di He ; Sheng-Guang Huang ; Hui-Jun Zhu ; Xiao-Guang Luo ; Kang-Han Liao ; Jie-Yao Zhang ; Ning Tan ; De-Yu LiSource :
- Pharmaceutical Biology [ 1388-0209 ] ; 2020.
Abstract
Url:
DOI: 10.1080/13880209.2020.1711783
PubMed: 31971852
PubMed Central: 7034059
Affiliations:
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PMC:7034059Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes</title>
<author><name sortKey="He, Shou Di" sort="He, Shou Di" uniqKey="He S" first="Shou-Di" last="He">Shou-Di He</name>
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<author><name sortKey="Zhu, Hui Jun" sort="Zhu, Hui Jun" uniqKey="Zhu H" first="Hui-Jun" last="Zhu">Hui-Jun Zhu</name>
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<author><name sortKey="Luo, Xiao Guang" sort="Luo, Xiao Guang" uniqKey="Luo X" first="Xiao-Guang" last="Luo">Xiao-Guang Luo</name>
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<author><name sortKey="Liao, Kang Han" sort="Liao, Kang Han" uniqKey="Liao K" first="Kang-Han" last="Liao">Kang-Han Liao</name>
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<author><name sortKey="Tan, Ning" sort="Tan, Ning" uniqKey="Tan N" first="Ning" last="Tan">Ning Tan</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes</title>
<author><name sortKey="He, Shou Di" sort="He, Shou Di" uniqKey="He S" first="Shou-Di" last="He">Shou-Di He</name>
<affiliation><nlm:aff id="AF0001"></nlm:aff>
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<author><name sortKey="Huang, Sheng Guang" sort="Huang, Sheng Guang" uniqKey="Huang S" first="Sheng-Guang" last="Huang">Sheng-Guang Huang</name>
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<author><name sortKey="Zhu, Hui Jun" sort="Zhu, Hui Jun" uniqKey="Zhu H" first="Hui-Jun" last="Zhu">Hui-Jun Zhu</name>
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</affiliation>
</author>
<author><name sortKey="Luo, Xiao Guang" sort="Luo, Xiao Guang" uniqKey="Luo X" first="Xiao-Guang" last="Luo">Xiao-Guang Luo</name>
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</affiliation>
</author>
<author><name sortKey="Liao, Kang Han" sort="Liao, Kang Han" uniqKey="Liao K" first="Kang-Han" last="Liao">Kang-Han Liao</name>
<affiliation><nlm:aff id="AF0001"></nlm:aff>
</affiliation>
</author>
<author><name sortKey="Zhang, Jie Yao" sort="Zhang, Jie Yao" uniqKey="Zhang J" first="Jie-Yao" last="Zhang">Jie-Yao Zhang</name>
<affiliation><nlm:aff id="AF0001"></nlm:aff>
</affiliation>
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<author><name sortKey="Tan, Ning" sort="Tan, Ning" uniqKey="Tan N" first="Ning" last="Tan">Ning Tan</name>
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<author><name sortKey="Li, De Yu" sort="Li, De Yu" uniqKey="Li D" first="De-Yu" last="Li">De-Yu Li</name>
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</affiliation>
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<series><title level="j">Pharmaceutical Biology</title>
<idno type="ISSN">1388-0209</idno>
<idno type="eISSN">1744-5116</idno>
<imprint><date when="2020">2020</date>
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<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<p><bold>Context:</bold>
Oridonin exhibits various pharmacological and physiological activities, including antioxidant, antibacterial, anti-inflammatory, pro-apoptotic, anticancer and neurological effects. However, its role in rheumatoid arthritis (RA) is yet to be revealed.</p>
<p><bold>Objective:</bold>
We evaluated the effects of oridonin on the survival and autophagy of RA-fibroblast-like synoviocytes (FLSs).</p>
<p><bold>Materials and methods:</bold>
RA-FLSs were treated with oridonin at serial concentrations of 0, 2, 4, 6, 8 and 10 µg/mL for 24, 48 and 72 h. Then, cell proliferation and apoptosis were measured. A GFP-LC3 plasmid was transfected into the cells to determine autophagy.</p>
<p><bold>Results:</bold>
Oridonin suppressed RA-FLS proliferation in a dose-dependent manner. The half maximal inhibitory concentrations (IC<sub>50</sub>
) of oridonin at 24, 48 and 72 h were 8.28, 7.88 and 8.35 µg/mL, respectively. Treatment with oridonin for 24 h increased apoptosis by 4.1%, and increased the protein levels of Bax and cleaved caspase-3 but significantly decreased the levels of IL-1β in the culture supernatant (<italic>p</italic>
< 0.05). In addition, 6 h of oridonin treatment significantly decreased the number of GFP-LC3 punctate dots and inhibited the protein levels of ATG5 and Beclin1 by 80.01% and 42.12%, respectively. Chloroquine (CQ) significantly reinforced the effects of oridonin on inhibition of autophagy, suppression of proliferation, and induction of apoptosis in RA-FLSs (<italic>p</italic>
< 0.05).</p>
<p><bold>Conclusions:</bold>
Our results indicate that treatment with oridonin in combination with CQ inhibits autophagy and cell proliferation and induces apoptosis in RA-FLSs more effectively than treatment oridonin alone. This finding indicates that oridonin is a potential therapeutic agent for RA.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Pharm Biol</journal-id>
<journal-id journal-id-type="iso-abbrev">Pharm Biol</journal-id>
<journal-id journal-id-type="publisher-id">IPHB</journal-id>
<journal-id journal-id-type="publisher-id">iphb20</journal-id>
<journal-title-group><journal-title>Pharmaceutical Biology</journal-title>
</journal-title-group>
<issn pub-type="ppub">1388-0209</issn>
<issn pub-type="epub">1744-5116</issn>
<publisher><publisher-name>Taylor & Francis</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">31971852</article-id>
<article-id pub-id-type="pmc">7034059</article-id>
<article-id pub-id-type="doi">10.1080/13880209.2020.1711783</article-id>
<article-id pub-id-type="publisher-id">1711783</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Oridonin suppresses autophagy and survival in rheumatoid arthritis fibroblast-like synoviocytes</article-title>
<alt-title alt-title-type="running-authors">S.-D. He et al.</alt-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>He</surname>
<given-names>Shou-Di</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Huang</surname>
<given-names>Sheng-Guang</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhu</surname>
<given-names>Hui-Jun</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Luo</surname>
<given-names>Xiao-Guang</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Liao</surname>
<given-names>Kang-Han</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Zhang</surname>
<given-names>Jie-Yao</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Tan</surname>
<given-names>Ning</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
</contrib>
<contrib contrib-type="author"><name><surname>Li</surname>
<given-names>De-Yu</given-names>
</name>
<xref ref-type="aff" rid="AF0001"></xref>
<xref ref-type="corresp" rid="AN0001"></xref>
</contrib>
<aff id="AF0001"><institution>Traditional Chinese Medicine Department of Rheumatism, Huazhong University of Science and Techology Union Shenzhen Hospital, Shenzhen Nanshan People's Hospital</institution>
, Shenzhen,<country>China</country>
</aff>
</contrib-group>
<author-notes><corresp id="AN0001">CONTACT De-Yu Li <email>ldeyu317@163.com</email>
<institution>Traditional Chinese Medicine Department of Rheumatism, Huazhong University of Science and Techology Union Shenzhen Hospital</institution>
, <addr-line>Shenzhen Nanshan People's Hospital, 89 Taoyuan Road, Nanshan District</addr-line>
, Shenzhen 518060, Guangdong, <country>China</country>
.</corresp>
</author-notes>
<pub-date pub-type="collection"><year>2020</year>
</pub-date>
<pub-date pub-type="epub"><day>23</day>
<month>1</month>
<year>2020</year>
</pub-date>
<volume>58</volume>
<issue>1</issue>
<fpage seq="19">146</fpage>
<lpage>151</lpage>
<history><date date-type="received"><day>05</day>
<month>7</month>
<year>2019</year>
</date>
<date date-type="rev-recd"><day>23</day>
<month>12</month>
<year>2019</year>
</date>
<date date-type="accepted"><day>31</day>
<month>12</month>
<year>2019</year>
</date>
</history>
<permissions><copyright-statement>© 2020 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group.</copyright-statement>
<copyright-year>2020</copyright-year>
<copyright-holder>The Author(s)</copyright-holder>
<license license-type="open-access" xlink:href="http://creativecommons.org/licenses/by/4.0/"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>
), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:href="IPHB_58_1711783.pdf"></self-uri>
<abstract><title>Abstract</title>
<p><bold>Context:</bold>
Oridonin exhibits various pharmacological and physiological activities, including antioxidant, antibacterial, anti-inflammatory, pro-apoptotic, anticancer and neurological effects. However, its role in rheumatoid arthritis (RA) is yet to be revealed.</p>
<p><bold>Objective:</bold>
We evaluated the effects of oridonin on the survival and autophagy of RA-fibroblast-like synoviocytes (FLSs).</p>
<p><bold>Materials and methods:</bold>
RA-FLSs were treated with oridonin at serial concentrations of 0, 2, 4, 6, 8 and 10 µg/mL for 24, 48 and 72 h. Then, cell proliferation and apoptosis were measured. A GFP-LC3 plasmid was transfected into the cells to determine autophagy.</p>
<p><bold>Results:</bold>
Oridonin suppressed RA-FLS proliferation in a dose-dependent manner. The half maximal inhibitory concentrations (IC<sub>50</sub>
) of oridonin at 24, 48 and 72 h were 8.28, 7.88 and 8.35 µg/mL, respectively. Treatment with oridonin for 24 h increased apoptosis by 4.1%, and increased the protein levels of Bax and cleaved caspase-3 but significantly decreased the levels of IL-1β in the culture supernatant (<italic>p</italic>
< 0.05). In addition, 6 h of oridonin treatment significantly decreased the number of GFP-LC3 punctate dots and inhibited the protein levels of ATG5 and Beclin1 by 80.01% and 42.12%, respectively. Chloroquine (CQ) significantly reinforced the effects of oridonin on inhibition of autophagy, suppression of proliferation, and induction of apoptosis in RA-FLSs (<italic>p</italic>
< 0.05).</p>
<p><bold>Conclusions:</bold>
Our results indicate that treatment with oridonin in combination with CQ inhibits autophagy and cell proliferation and induces apoptosis in RA-FLSs more effectively than treatment oridonin alone. This finding indicates that oridonin is a potential therapeutic agent for RA.</p>
</abstract>
<kwd-group kwd-group-type="author"><title>KEYWORD</title>
<kwd>Chloroquine Oridonin</kwd>
<kwd>rheumatoid arthritis</kwd>
<kwd>autophagy</kwd>
<kwd>chloroquine</kwd>
</kwd-group>
<funding-group><funding-statement>This work was supported by the Guangdong Science and Technology Research Project (2017A020215129); Shenzhen Scientific Technology Basic Research Project (JCYJ20160429183052202); Shenzhen Health and Family Planning Research Project (201606050); and the Shenzhen Nanshan District Scientific Research Project (2015021).</funding-statement>
</funding-group>
<counts><fig-count count="4"></fig-count>
<table-count count="0"></table-count>
<page-count count="6"></page-count>
<word-count count="4086"></word-count>
</counts>
</article-meta>
</front>
</pmc>
<affiliations><list></list>
<tree><noCountry><name sortKey="He, Shou Di" sort="He, Shou Di" uniqKey="He S" first="Shou-Di" last="He">Shou-Di He</name>
<name sortKey="Huang, Sheng Guang" sort="Huang, Sheng Guang" uniqKey="Huang S" first="Sheng-Guang" last="Huang">Sheng-Guang Huang</name>
<name sortKey="Li, De Yu" sort="Li, De Yu" uniqKey="Li D" first="De-Yu" last="Li">De-Yu Li</name>
<name sortKey="Liao, Kang Han" sort="Liao, Kang Han" uniqKey="Liao K" first="Kang-Han" last="Liao">Kang-Han Liao</name>
<name sortKey="Luo, Xiao Guang" sort="Luo, Xiao Guang" uniqKey="Luo X" first="Xiao-Guang" last="Luo">Xiao-Guang Luo</name>
<name sortKey="Tan, Ning" sort="Tan, Ning" uniqKey="Tan N" first="Ning" last="Tan">Ning Tan</name>
<name sortKey="Zhang, Jie Yao" sort="Zhang, Jie Yao" uniqKey="Zhang J" first="Jie-Yao" last="Zhang">Jie-Yao Zhang</name>
<name sortKey="Zhu, Hui Jun" sort="Zhu, Hui Jun" uniqKey="Zhu H" first="Hui-Jun" last="Zhu">Hui-Jun Zhu</name>
</noCountry>
</tree>
</affiliations>
</record>
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