Tanshinone IIA Downregulates HMGB1 and TLR4 Expression in a Spinal Nerve Ligation Model of Neuropathic Pain
Fifty-four Sprague-Dawley rats weighing 200~240 g were randomly divided into sham-operated group (sham group), vehicle-treated SNL group (model group), and Tan IIA-treated SNL group (Tan IIA group). Tan IIA was administered intraperitoneally to rats in the Tan IIA-treated group at a dose of 30 mg/kg...
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| description | Fifty-four Sprague-Dawley rats weighing 200~240 g were randomly divided into sham-operated group (sham group), vehicle-treated SNL group (model group), and Tan IIA-treated SNL group (Tan IIA group). Tan IIA was administered intraperitoneally to rats in the Tan IIA-treated group at a dose of 30 mg/kg daily for 14 days after SNL surgery. Paw withdrawal mechanical thresholds (PWTs) and paw withdrawal thermal latencies (PWLs) were measured. High-mobility group box 1 (HMGB1) and Toll-like Receptor 4 (TLR4) mRNA and protein expression in the spinal cord were measured. Tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10) in the spinal cord were measured, too. Both the mechanical and heat pain thresholds were significantly decreased. After Tan IIA treatment, HMGB1, and TLR4 mRNA and protein levels, the expression of TNF-α and IF-1β was reduced significantly. In conclusion, Tanshinone IIA reversed SNL-induced thermal hyperalgesia and mechanical allodynia and downregulated HMGB1 and TLR4 levels and inhibited the HMGB1-TLR4 pathway. Tanshinone IIA inhibited TNF-α and IL-1β expression but not IF-10 expression in the spinal cords of SNL rats. These results indicate that Tanshinone IIA inhibited SNL-induced neuropathic pain via multiple effects, and targeting the HMGB1-TLR4 pathway could serve as the basis of new antinociceptive agents. |
| doi_str_mv | 10.1155/2014/639563 |
| format | Article |
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Tan IIA was administered intraperitoneally to rats in the Tan IIA-treated group at a dose of 30 mg/kg daily for 14 days after SNL surgery. Paw withdrawal mechanical thresholds (PWTs) and paw withdrawal thermal latencies (PWLs) were measured. High-mobility group box 1 (HMGB1) and Toll-like Receptor 4 (TLR4) mRNA and protein expression in the spinal cord were measured. Tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10) in the spinal cord were measured, too. Both the mechanical and heat pain thresholds were significantly decreased. After Tan IIA treatment, HMGB1, and TLR4 mRNA and protein levels, the expression of TNF-α and IF-1β was reduced significantly. In conclusion, Tanshinone IIA reversed SNL-induced thermal hyperalgesia and mechanical allodynia and downregulated HMGB1 and TLR4 levels and inhibited the HMGB1-TLR4 pathway. Tanshinone IIA inhibited TNF-α and IL-1β expression but not IF-10 expression in the spinal cords of SNL rats. These results indicate that Tanshinone IIA inhibited SNL-induced neuropathic pain via multiple effects, and targeting the HMGB1-TLR4 pathway could serve as the basis of new antinociceptive agents.</description><identifier>ISSN: 1741-427X</identifier><identifier>EISSN: 1741-4288</identifier><identifier>DOI: 10.1155/2014/639563</identifier><identifier>PMID: 25120576</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Care and treatment ; Chinese medicine ; Chromatin ; Chronic pain ; Cytokines ; Gene expression ; Health aspects ; HMGB1 protein ; Hyperalgesia ; Interleukin 1 ; Interleukin 10 ; mRNA ; Neuralgia ; Neurosciences ; Pain ; Pain perception ; Physiological aspects ; Properties ; Quinone ; Rats ; Rodents ; Spinal cord ; Surgery ; Thresholds ; TLR4 protein ; Toll-like receptors ; Tumor necrosis factor-α ; Tumors</subject><ispartof>Evidence-based complementary and alternative medicine, 2014-01, Vol.2014 (2014), p.1-8</ispartof><rights>Copyright © 2014 Yu-Qing Ma et al.</rights><rights>COPYRIGHT 2014 John Wiley & Sons, Inc.</rights><rights>Copyright © 2014 Yu-Qing Ma et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2014 Yu-Qing Ma et al. 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c561t-b0e3a1f89a5e7a1ae9b9755d3fa2ee62a3077a6a0ead67684aa2c7185d7df38a3</citedby><cites>FETCH-LOGICAL-c561t-b0e3a1f89a5e7a1ae9b9755d3fa2ee62a3077a6a0ead67684aa2c7185d7df38a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120799/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4120799/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25120576$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sandner-Kiesling, Andreas</contributor><contributor>Andreas Sandner-Kiesling</contributor><creatorcontrib>Wu, Zhi-Wei</creatorcontrib><creatorcontrib>Leng, Yu-Fang</creatorcontrib><creatorcontrib>Chen, Yi-Rong</creatorcontrib><creatorcontrib>Ma, Yu-Qing</creatorcontrib><title>Tanshinone IIA Downregulates HMGB1 and TLR4 Expression in a Spinal Nerve Ligation Model of Neuropathic Pain</title><title>Evidence-based complementary and alternative medicine</title><addtitle>Evid Based Complement Alternat Med</addtitle><description>Fifty-four Sprague-Dawley rats weighing 200~240 g were randomly divided into sham-operated group (sham group), vehicle-treated SNL group (model group), and Tan IIA-treated SNL group (Tan IIA group). Tan IIA was administered intraperitoneally to rats in the Tan IIA-treated group at a dose of 30 mg/kg daily for 14 days after SNL surgery. Paw withdrawal mechanical thresholds (PWTs) and paw withdrawal thermal latencies (PWLs) were measured. High-mobility group box 1 (HMGB1) and Toll-like Receptor 4 (TLR4) mRNA and protein expression in the spinal cord were measured. Tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10) in the spinal cord were measured, too. Both the mechanical and heat pain thresholds were significantly decreased. After Tan IIA treatment, HMGB1, and TLR4 mRNA and protein levels, the expression of TNF-α and IF-1β was reduced significantly. In conclusion, Tanshinone IIA reversed SNL-induced thermal hyperalgesia and mechanical allodynia and downregulated HMGB1 and TLR4 levels and inhibited the HMGB1-TLR4 pathway. Tanshinone IIA inhibited TNF-α and IL-1β expression but not IF-10 expression in the spinal cords of SNL rats. These results indicate that Tanshinone IIA inhibited SNL-induced neuropathic pain via multiple effects, and targeting the HMGB1-TLR4 pathway could serve as the basis of new antinociceptive agents.</description><subject>Care and treatment</subject><subject>Chinese medicine</subject><subject>Chromatin</subject><subject>Chronic pain</subject><subject>Cytokines</subject><subject>Gene expression</subject><subject>Health aspects</subject><subject>HMGB1 protein</subject><subject>Hyperalgesia</subject><subject>Interleukin 1</subject><subject>Interleukin 10</subject><subject>mRNA</subject><subject>Neuralgia</subject><subject>Neurosciences</subject><subject>Pain</subject><subject>Pain perception</subject><subject>Physiological aspects</subject><subject>Properties</subject><subject>Quinone</subject><subject>Rats</subject><subject>Rodents</subject><subject>Spinal cord</subject><subject>Surgery</subject><subject>Thresholds</subject><subject>TLR4 protein</subject><subject>Toll-like receptors</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><issn>1741-427X</issn><issn>1741-4288</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkc1vEzEQxVcIREvhxB1Z4oJAof5Yf-ylUiiljZQCgiBxsya7s4nLxl7s3Rb-exylhMKJk0een97MvFcUTxl9zZiUx5yy8liJSipxrzhkumSTkhtzf1_rrwfFo5SuKOWV1vphccAl41RqdVh8W4BPa-eDRzKbTcnbcOMjrsYOBkzk4vL8DSPgG7KYfyrJ2Y8-YkoueOI8AfK5dx468h7jNZK5W8GwbV2GBjsS2vw_xtDDsHY1-QjOPy4etNAlfHL7HhVf3p0tTi8m8w_ns9PpfFJLxYbJkqIA1poKJGpggNWy0lI2ogWOqDgIqjUooAiN0sqUALzWzMhGN60wII6Kk51uPy432NTohwid7aPbQPxpAzj7d8e7tV2Fa1tmV3RVZYEXtwIxfB8xDXbjUo1dBx7DmGx2XWhalXqLPv8HvQpjzK4ky6mihom84h9qBR1a59uQ59ZbUTstmWZUCWMy9WpH1TGkFLHdr8yo3UZtt1HbXdSZfnb3yj37O9sMvNwBOd4Gbtz_qWFGsIU7MDPacPELuLW5EQ</recordid><startdate>20140101</startdate><enddate>20140101</enddate><creator>Wu, Zhi-Wei</creator><creator>Leng, Yu-Fang</creator><creator>Chen, Yi-Rong</creator><creator>Ma, Yu-Qing</creator><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M2M</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140101</creationdate><title>Tanshinone IIA Downregulates HMGB1 and TLR4 Expression in a Spinal Nerve Ligation Model of Neuropathic Pain</title><author>Wu, Zhi-Wei ; 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Tan IIA was administered intraperitoneally to rats in the Tan IIA-treated group at a dose of 30 mg/kg daily for 14 days after SNL surgery. Paw withdrawal mechanical thresholds (PWTs) and paw withdrawal thermal latencies (PWLs) were measured. High-mobility group box 1 (HMGB1) and Toll-like Receptor 4 (TLR4) mRNA and protein expression in the spinal cord were measured. Tumour necrosis factor alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-10 (IL-10) in the spinal cord were measured, too. Both the mechanical and heat pain thresholds were significantly decreased. After Tan IIA treatment, HMGB1, and TLR4 mRNA and protein levels, the expression of TNF-α and IF-1β was reduced significantly. In conclusion, Tanshinone IIA reversed SNL-induced thermal hyperalgesia and mechanical allodynia and downregulated HMGB1 and TLR4 levels and inhibited the HMGB1-TLR4 pathway. Tanshinone IIA inhibited TNF-α and IL-1β expression but not IF-10 expression in the spinal cords of SNL rats. These results indicate that Tanshinone IIA inhibited SNL-induced neuropathic pain via multiple effects, and targeting the HMGB1-TLR4 pathway could serve as the basis of new antinociceptive agents.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>25120576</pmid><doi>10.1155/2014/639563</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Care and treatment Chinese medicine Chromatin Chronic pain Cytokines Gene expression Health aspects HMGB1 protein Hyperalgesia Interleukin 1 Interleukin 10 mRNA Neuralgia Neurosciences Pain Pain perception Physiological aspects Properties Quinone Rats Rodents Spinal cord Surgery Thresholds TLR4 protein Toll-like receptors Tumor necrosis factor-α Tumors |
| title | Tanshinone IIA Downregulates HMGB1 and TLR4 Expression in a Spinal Nerve Ligation Model of Neuropathic Pain |
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