Cedrol protects against chronic constriction injury-induced neuropathic pain through inhibiting oxidative stress and inflammation
Injured somatosensory nervous system cause neuropathic pain which is quite difficult to treat using current approaches. It is therefore important to find new therapeutic options. We have analyzed cedrol effect on chronic constriction injury (CCI) induced neuropathic pain in rats. The mechanical and...
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| Veröffentlicht in: | Metabolic brain disease 2020-10, Vol.35 (7), p.1119-1126 |
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| creator | Sakhaee, Mohammad Hossein Sayyadi, Seyed Amir Hossein Sakhaee, Nader Sadeghnia, Hamid R. Hosseinzadeh, Hossein Nourbakhsh, Fahimeh Forouzanfar, Fatemeh |
| description | Injured somatosensory nervous system cause neuropathic pain which is quite difficult to treat using current approaches. It is therefore important to find new therapeutic options. We have analyzed cedrol effect on chronic constriction injury (CCI) induced neuropathic pain in rats. The mechanical and thermal hypersensitivity were evaluated using the von Frey filament, radiant heat and acetone drop methods. The changes in the levels of biomarkers of oxidative stress including malondialdehyde (MDA) and total thiol (SH), as well as inflammatory mediators including Tumour Necrosis Factor alpha (TNF-α) and Interleukin 6 (IL-6) were estimated in the lumbar portion (L4–L6) of neuropathic rats. Administration of cedrol attenuated the CCI-induced mechanical and thermal hypersensitivity. CCI produced an increase in MDA along with a reduction in SH levels in the spinal cord of the CCI rats. Reduced levels of SH were restored by cedrol. Also, the levels of MDA were reduced in the cedrol-treated CCI rats compared to the untreated CCI rats. Besides, level of TNF-α and IL-6 increased in the spinal cord of CCI group and cedrol could reverse it. The current study showed that cedrol attenuates neuropathic pain in CCI rats by inhibition of inflammatory response and attenuation of oxidative stress. |
| doi_str_mv | 10.1007/s11011-020-00581-8 |
| format | Article |
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It is therefore important to find new therapeutic options. We have analyzed cedrol effect on chronic constriction injury (CCI) induced neuropathic pain in rats. The mechanical and thermal hypersensitivity were evaluated using the von Frey filament, radiant heat and acetone drop methods. The changes in the levels of biomarkers of oxidative stress including malondialdehyde (MDA) and total thiol (SH), as well as inflammatory mediators including Tumour Necrosis Factor alpha (TNF-α) and Interleukin 6 (IL-6) were estimated in the lumbar portion (L4–L6) of neuropathic rats. Administration of cedrol attenuated the CCI-induced mechanical and thermal hypersensitivity. CCI produced an increase in MDA along with a reduction in SH levels in the spinal cord of the CCI rats. Reduced levels of SH were restored by cedrol. Also, the levels of MDA were reduced in the cedrol-treated CCI rats compared to the untreated CCI rats. Besides, level of TNF-α and IL-6 increased in the spinal cord of CCI group and cedrol could reverse it. The current study showed that cedrol attenuates neuropathic pain in CCI rats by inhibition of inflammatory response and attenuation of oxidative stress.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-020-00581-8</identifier><identifier>PMID: 32472224</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acetone ; Animals ; Attenuation ; Biochemistry ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Constrictions ; Hypersensitivity ; Inflammation ; Inflammation - drug therapy ; Inflammation - metabolism ; Inflammatory response ; Injuries ; Injury analysis ; Interleukin 6 ; Interleukin-6 - metabolism ; Male ; Malondialdehyde ; Malondialdehyde - metabolism ; Metabolic Diseases ; Nervous system ; Neuralgia ; Neuralgia - metabolism ; Neuralgia - prevention & control ; Neurology ; Neurosciences ; Oncology ; Original Article ; Oxidative stress ; Oxidative Stress - drug effects ; Pain ; Pain Threshold - drug effects ; Polycyclic Sesquiterpenes - pharmacology ; Polycyclic Sesquiterpenes - therapeutic use ; Protective Agents - pharmacology ; Protective Agents - therapeutic use ; Rats ; Rats, Wistar ; Sensory Receptor Cells - drug effects ; Sensory Receptor Cells - metabolism ; Spinal cord ; Spinal Cord - drug effects ; Spinal Cord - metabolism ; Sulfhydryl Compounds - metabolism ; Tumor Necrosis Factor-alpha - metabolism ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; Tumors</subject><ispartof>Metabolic brain disease, 2020-10, Vol.35 (7), p.1119-1126</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2020.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c441t-33f22bdac468ea54839df10dced2969cea124d94213997b82a970a13ec592023</citedby><cites>FETCH-LOGICAL-c441t-33f22bdac468ea54839df10dced2969cea124d94213997b82a970a13ec592023</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11011-020-00581-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11011-020-00581-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,778,782,27907,27908,41471,42540,51302</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32472224$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sakhaee, Mohammad Hossein</creatorcontrib><creatorcontrib>Sayyadi, Seyed Amir Hossein</creatorcontrib><creatorcontrib>Sakhaee, Nader</creatorcontrib><creatorcontrib>Sadeghnia, Hamid R.</creatorcontrib><creatorcontrib>Hosseinzadeh, Hossein</creatorcontrib><creatorcontrib>Nourbakhsh, Fahimeh</creatorcontrib><creatorcontrib>Forouzanfar, Fatemeh</creatorcontrib><title>Cedrol protects against chronic constriction injury-induced neuropathic pain through inhibiting oxidative stress and inflammation</title><title>Metabolic brain disease</title><addtitle>Metab Brain Dis</addtitle><addtitle>Metab Brain Dis</addtitle><description>Injured somatosensory nervous system cause neuropathic pain which is quite difficult to treat using current approaches. It is therefore important to find new therapeutic options. We have analyzed cedrol effect on chronic constriction injury (CCI) induced neuropathic pain in rats. The mechanical and thermal hypersensitivity were evaluated using the von Frey filament, radiant heat and acetone drop methods. The changes in the levels of biomarkers of oxidative stress including malondialdehyde (MDA) and total thiol (SH), as well as inflammatory mediators including Tumour Necrosis Factor alpha (TNF-α) and Interleukin 6 (IL-6) were estimated in the lumbar portion (L4–L6) of neuropathic rats. Administration of cedrol attenuated the CCI-induced mechanical and thermal hypersensitivity. CCI produced an increase in MDA along with a reduction in SH levels in the spinal cord of the CCI rats. Reduced levels of SH were restored by cedrol. Also, the levels of MDA were reduced in the cedrol-treated CCI rats compared to the untreated CCI rats. Besides, level of TNF-α and IL-6 increased in the spinal cord of CCI group and cedrol could reverse it. The current study showed that cedrol attenuates neuropathic pain in CCI rats by inhibition of inflammatory response and attenuation of oxidative stress.</description><subject>Acetone</subject><subject>Animals</subject><subject>Attenuation</subject><subject>Biochemistry</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Constrictions</subject><subject>Hypersensitivity</subject><subject>Inflammation</subject><subject>Inflammation - drug therapy</subject><subject>Inflammation - metabolism</subject><subject>Inflammatory response</subject><subject>Injuries</subject><subject>Injury analysis</subject><subject>Interleukin 6</subject><subject>Interleukin-6 - metabolism</subject><subject>Male</subject><subject>Malondialdehyde</subject><subject>Malondialdehyde - metabolism</subject><subject>Metabolic Diseases</subject><subject>Nervous system</subject><subject>Neuralgia</subject><subject>Neuralgia - metabolism</subject><subject>Neuralgia - prevention & control</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pain</subject><subject>Pain Threshold - drug effects</subject><subject>Polycyclic Sesquiterpenes - pharmacology</subject><subject>Polycyclic Sesquiterpenes - therapeutic use</subject><subject>Protective Agents - pharmacology</subject><subject>Protective Agents - therapeutic use</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Sensory Receptor Cells - drug effects</subject><subject>Sensory Receptor Cells - metabolism</subject><subject>Spinal cord</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - metabolism</subject><subject>Sulfhydryl Compounds - metabolism</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>Tumors</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kM1uWyEQhVHVqnbcvkAXEVLXJMPP9YVlZSVtJUvdeI8wcG0sGxzgVskybx5cO8muq9FovnMOHIS-UbihAP1toRQoJcCAAHSSEvkBTWnXc9LzefcRTUHKjvRCwQRdlbIDAN5R9RlNOBM9Y0xM0fPCu5z2-JhT9bYWbDYmxFKx3eYUg8U2tS0HW0OKOMTdmJ9IiG603uHox5yOpm4bd2wyXJto3Gwbtw3rUEPc4PQYnKnhr8fNxpcWEF27D3tzOJiT6Rf0aTD74r9e5gyt7u9Wi19k-efn78WPJbFC0Eo4HxhbO2PFXHrTCcmVGyi49g6m5sp6Q5lwSjDKlerXkhnVg6Hc204xYHyGvp9t208fRl-q3qUxx5aomRDAGVVSNIqdKZtTKdkP-pjDweQnTUGfStfn0nUrXf8rXcsmur5Yj-uDd2-S15YbwM9Aaae48fk9-z-2L25gj-c</recordid><startdate>20201001</startdate><enddate>20201001</enddate><creator>Sakhaee, Mohammad Hossein</creator><creator>Sayyadi, Seyed Amir Hossein</creator><creator>Sakhaee, Nader</creator><creator>Sadeghnia, Hamid R.</creator><creator>Hosseinzadeh, Hossein</creator><creator>Nourbakhsh, Fahimeh</creator><creator>Forouzanfar, Fatemeh</creator><general>Springer US</general><general>Springer Nature 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>3V.</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope></search><sort><creationdate>20201001</creationdate><title>Cedrol protects against chronic constriction injury-induced neuropathic pain through inhibiting oxidative stress and inflammation</title><author>Sakhaee, Mohammad Hossein ; Sayyadi, Seyed Amir Hossein ; Sakhaee, Nader ; Sadeghnia, Hamid R. ; Hosseinzadeh, Hossein ; Nourbakhsh, Fahimeh ; Forouzanfar, Fatemeh</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-33f22bdac468ea54839df10dced2969cea124d94213997b82a970a13ec592023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Acetone</topic><topic>Animals</topic><topic>Attenuation</topic><topic>Biochemistry</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Constrictions</topic><topic>Hypersensitivity</topic><topic>Inflammation</topic><topic>Inflammation - drug therapy</topic><topic>Inflammation - metabolism</topic><topic>Inflammatory response</topic><topic>Injuries</topic><topic>Injury analysis</topic><topic>Interleukin 6</topic><topic>Interleukin-6 - metabolism</topic><topic>Male</topic><topic>Malondialdehyde</topic><topic>Malondialdehyde - metabolism</topic><topic>Metabolic Diseases</topic><topic>Nervous system</topic><topic>Neuralgia</topic><topic>Neuralgia - metabolism</topic><topic>Neuralgia - prevention & control</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Pain</topic><topic>Pain Threshold - drug effects</topic><topic>Polycyclic Sesquiterpenes - pharmacology</topic><topic>Polycyclic Sesquiterpenes - therapeutic use</topic><topic>Protective Agents - pharmacology</topic><topic>Protective Agents - therapeutic use</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Sensory Receptor Cells - drug effects</topic><topic>Sensory Receptor Cells - metabolism</topic><topic>Spinal cord</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - metabolism</topic><topic>Sulfhydryl Compounds - metabolism</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><topic>Tumors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sakhaee, Mohammad Hossein</creatorcontrib><creatorcontrib>Sayyadi, Seyed Amir Hossein</creatorcontrib><creatorcontrib>Sakhaee, Nader</creatorcontrib><creatorcontrib>Sadeghnia, Hamid R.</creatorcontrib><creatorcontrib>Hosseinzadeh, Hossein</creatorcontrib><creatorcontrib>Nourbakhsh, Fahimeh</creatorcontrib><creatorcontrib>Forouzanfar, Fatemeh</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Psychology Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sakhaee, Mohammad Hossein</au><au>Sayyadi, Seyed Amir Hossein</au><au>Sakhaee, Nader</au><au>Sadeghnia, Hamid R.</au><au>Hosseinzadeh, Hossein</au><au>Nourbakhsh, Fahimeh</au><au>Forouzanfar, Fatemeh</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cedrol protects against chronic constriction injury-induced neuropathic pain through inhibiting oxidative stress and inflammation</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2020-10-01</date><risdate>2020</risdate><volume>35</volume><issue>7</issue><spage>1119</spage><epage>1126</epage><pages>1119-1126</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>Injured somatosensory nervous system cause neuropathic pain which is quite difficult to treat using current approaches. It is therefore important to find new therapeutic options. We have analyzed cedrol effect on chronic constriction injury (CCI) induced neuropathic pain in rats. The mechanical and thermal hypersensitivity were evaluated using the von Frey filament, radiant heat and acetone drop methods. The changes in the levels of biomarkers of oxidative stress including malondialdehyde (MDA) and total thiol (SH), as well as inflammatory mediators including Tumour Necrosis Factor alpha (TNF-α) and Interleukin 6 (IL-6) were estimated in the lumbar portion (L4–L6) of neuropathic rats. Administration of cedrol attenuated the CCI-induced mechanical and thermal hypersensitivity. CCI produced an increase in MDA along with a reduction in SH levels in the spinal cord of the CCI rats. Reduced levels of SH were restored by cedrol. Also, the levels of MDA were reduced in the cedrol-treated CCI rats compared to the untreated CCI rats. Besides, level of TNF-α and IL-6 increased in the spinal cord of CCI group and cedrol could reverse it. The current study showed that cedrol attenuates neuropathic pain in CCI rats by inhibition of inflammatory response and attenuation of oxidative stress.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>32472224</pmid><doi>10.1007/s11011-020-00581-8</doi><tpages>8</tpages></addata></record> |
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| subjects | Acetone Animals Attenuation Biochemistry Biomarkers Biomedical and Life Sciences Biomedicine Constrictions Hypersensitivity Inflammation Inflammation - drug therapy Inflammation - metabolism Inflammatory response Injuries Injury analysis Interleukin 6 Interleukin-6 - metabolism Male Malondialdehyde Malondialdehyde - metabolism Metabolic Diseases Nervous system Neuralgia Neuralgia - metabolism Neuralgia - prevention & control Neurology Neurosciences Oncology Original Article Oxidative stress Oxidative Stress - drug effects Pain Pain Threshold - drug effects Polycyclic Sesquiterpenes - pharmacology Polycyclic Sesquiterpenes - therapeutic use Protective Agents - pharmacology Protective Agents - therapeutic use Rats Rats, Wistar Sensory Receptor Cells - drug effects Sensory Receptor Cells - metabolism Spinal cord Spinal Cord - drug effects Spinal Cord - metabolism Sulfhydryl Compounds - metabolism Tumor Necrosis Factor-alpha - metabolism Tumor necrosis factor-TNF Tumor necrosis factor-α Tumors |
| title | Cedrol protects against chronic constriction injury-induced neuropathic pain through inhibiting oxidative stress and inflammation |
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