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Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes
Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperat...
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Published in: | Chinese journal of natural medicines 2017-03, Vol.15 (3), p.178-191 |
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creator | JIANG, Jing-Fei LEI, Fan YUAN, Zhi-Yi WANG, Yu-Gang WANG, Xin-Pei YAN, Xiao-Jin YU, Xuan XING, Dong-Ming DU, Li-Jun |
description | Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments. |
doi_str_mv | 10.1016/S1875-5364(17)30034-1 |
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The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.</description><identifier>ISSN: 1875-5364</identifier><identifier>EISSN: 1875-5364</identifier><identifier>DOI: 10.1016/S1875-5364(17)30034-1</identifier><identifier>PMID: 28411686</identifier><language>eng</language><publisher>China: Elsevier B.V</publisher><subject>Animals ; Berberine ; Berberine - pharmacology ; Heat Stress Disorders - drug therapy ; Heat Stress Disorders - genetics ; Heat Stress Disorders - metabolism ; Hot Temperature ; HSP70 ; HSP70 Heat-Shock Proteins - genetics ; HSP70 Heat-Shock Proteins - metabolism ; Humans ; Hyperthermia ; Male ; Mice ; Mice, Inbred ICR ; TATA box ; TATA Box - drug effects ; TNFα ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Chinese journal of natural medicines, 2017-03, Vol.15 (3), p.178-191</ispartof><rights>2017 China Pharmaceutical University</rights><rights>Copyright © 2017 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c365t-5209c794d36bbbc172842bf4c9996a15899545a7669d2109d13e63da75aeaf7d3</citedby><cites>FETCH-LOGICAL-c365t-5209c794d36bbbc172842bf4c9996a15899545a7669d2109d13e63da75aeaf7d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28411686$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>JIANG, Jing-Fei</creatorcontrib><creatorcontrib>LEI, Fan</creatorcontrib><creatorcontrib>YUAN, Zhi-Yi</creatorcontrib><creatorcontrib>WANG, Yu-Gang</creatorcontrib><creatorcontrib>WANG, Xin-Pei</creatorcontrib><creatorcontrib>YAN, Xiao-Jin</creatorcontrib><creatorcontrib>YU, Xuan</creatorcontrib><creatorcontrib>XING, Dong-Ming</creatorcontrib><creatorcontrib>DU, Li-Jun</creatorcontrib><title>Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes</title><title>Chinese journal of natural medicines</title><addtitle>Chin J Nat Med</addtitle><description>Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.</description><subject>Animals</subject><subject>Berberine</subject><subject>Berberine - pharmacology</subject><subject>Heat Stress Disorders - drug therapy</subject><subject>Heat Stress Disorders - genetics</subject><subject>Heat Stress Disorders - metabolism</subject><subject>Hot Temperature</subject><subject>HSP70</subject><subject>HSP70 Heat-Shock Proteins - genetics</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Humans</subject><subject>Hyperthermia</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred ICR</subject><subject>TATA box</subject><subject>TATA Box - drug effects</subject><subject>TNFα</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>1875-5364</issn><issn>1875-5364</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><recordid>eNqFkM1OGzEQgC1UVBDwCEW-AYcFT7y211yqKCoFiUKlpGfLa882Rptdam-gPBYvwjPVIWnUWy1LM7K--fFHyCdg58BAXkyhUqIQXJanoM44Y7wsYIfsb58__JPvkaOUHlg-UgAH-ZHsjaoSQFZynzx8Qze3XUgLuuw8xvYldD9pjTHf0OFJotg06IZE-45eT78rdjG7u3p7XdN0jnagaYiY0iWd9DFia4eQ0ecwzOkwRzobz8a07n9jOiS7jW0THm3iAflx9WU2uS5u77_eTMa3heNSDIUYMe2ULj2XdV07UHnZUd2UTmstLYhKa1EKq6TUfgRMe-AoubdKWLSN8vyAnK77Psb-1xLTYBYhOWxb22G_TAaqqtJC55BRsUZd7FOK2JjHGBY2vhhgZmXavJs2K40GlHk3bSDXHW9GLOsF-m3VX68Z-LwGMH_0KWA0yQXsHPoQs03j-_CfEX8A0aKNAg</recordid><startdate>201703</startdate><enddate>201703</enddate><creator>JIANG, Jing-Fei</creator><creator>LEI, Fan</creator><creator>YUAN, Zhi-Yi</creator><creator>WANG, Yu-Gang</creator><creator>WANG, Xin-Pei</creator><creator>YAN, Xiao-Jin</creator><creator>YU, Xuan</creator><creator>XING, Dong-Ming</creator><creator>DU, Li-Jun</creator><general>Elsevier B.V</general><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>201703</creationdate><title>Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes</title><author>JIANG, Jing-Fei ; LEI, Fan ; YUAN, Zhi-Yi ; WANG, Yu-Gang ; WANG, Xin-Pei ; YAN, Xiao-Jin ; YU, Xuan ; XING, Dong-Ming ; DU, Li-Jun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c365t-5209c794d36bbbc172842bf4c9996a15899545a7669d2109d13e63da75aeaf7d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Berberine</topic><topic>Berberine - pharmacology</topic><topic>Heat Stress Disorders - drug therapy</topic><topic>Heat Stress Disorders - genetics</topic><topic>Heat Stress Disorders - metabolism</topic><topic>Hot Temperature</topic><topic>HSP70</topic><topic>HSP70 Heat-Shock Proteins - genetics</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Humans</topic><topic>Hyperthermia</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred ICR</topic><topic>TATA box</topic><topic>TATA Box - drug effects</topic><topic>TNFα</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>online_resources</toplevel><creatorcontrib>JIANG, Jing-Fei</creatorcontrib><creatorcontrib>LEI, Fan</creatorcontrib><creatorcontrib>YUAN, Zhi-Yi</creatorcontrib><creatorcontrib>WANG, Yu-Gang</creatorcontrib><creatorcontrib>WANG, Xin-Pei</creatorcontrib><creatorcontrib>YAN, Xiao-Jin</creatorcontrib><creatorcontrib>YU, Xuan</creatorcontrib><creatorcontrib>XING, Dong-Ming</creatorcontrib><creatorcontrib>DU, Li-Jun</creatorcontrib><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>Chinese journal of natural medicines</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>JIANG, Jing-Fei</au><au>LEI, Fan</au><au>YUAN, Zhi-Yi</au><au>WANG, Yu-Gang</au><au>WANG, Xin-Pei</au><au>YAN, Xiao-Jin</au><au>YU, Xuan</au><au>XING, Dong-Ming</au><au>DU, Li-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes</atitle><jtitle>Chinese journal of natural medicines</jtitle><addtitle>Chin J Nat Med</addtitle><date>2017-03</date><risdate>2017</risdate><volume>15</volume><issue>3</issue><spage>178</spage><epage>191</epage><pages>178-191</pages><issn>1875-5364</issn><eissn>1875-5364</eissn><notes>ObjectType-Article-1</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-2</notes><notes>content type line 23</notes><abstract>Heat stress can stimulate an increase in body temperature, which is correlated with increased expression of heat shock protein 70 (HSP70) and tumor necrosis factor α (TNFα). The exact mechanism underlying the HSP70 and TNFα induction is unclear. Berberine (BBR) can significantly inhibit the temperature rise caused by heat stress, but the mechanism responsible for the BBR effect on HSP70 and TNFα signaling has not been investigated. The aim of the present study was to explore the relationship between the expression of HSP70 and TNFα and the effects of BBR under heat conditions, using in vivo and in vitro models. The expression levels of HSP70 and TNFα were determined using RT-PCR and Western blotting analyses. The results showed that the levels of HSP70 and TNFα were up-regulated under heat conditions (40 °C). HSP70 acted as a chaperone to maintain TNFα homeostasis with rising the temperature, but knockdown of HSP70 could not down-regulate the level of TNFα. Furthermore, TNFα could not influence the expression of HSP70 under normal and heat conditions. BBR targeted both HSP70 and TNFα by suppressing their gene transcription, thereby decreasing body temperature under heat conditions. In conclusion, BBR has a potential to be developed as a therapeutic strategy for suppressing the thermal effects in hot environments.</abstract><cop>China</cop><pub>Elsevier B.V</pub><pmid>28411686</pmid><doi>10.1016/S1875-5364(17)30034-1</doi><tpages>14</tpages></addata></record> |
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subjects | Animals Berberine Berberine - pharmacology Heat Stress Disorders - drug therapy Heat Stress Disorders - genetics Heat Stress Disorders - metabolism Hot Temperature HSP70 HSP70 Heat-Shock Proteins - genetics HSP70 Heat-Shock Proteins - metabolism Humans Hyperthermia Male Mice Mice, Inbred ICR TATA box TATA Box - drug effects TNFα Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism |
title | Mechanism underlying berberine's effects on HSP70/TNFα under heat stress: Correlation with the TATA boxes |
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