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Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a Cardioprotective Agent in the Future Treatment
Ischemia/reperfusion (I/R) is a pivotal mechanism of organ injury during clinical stetting for example for cardiopulmonary bypasses. The generation of reactive oxygen species (ROS) during I/R induces oxidative stress that promotes endothelial dysfunction, DNA dissociation and local inflammation. In...
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| Published in: | Frontiers in bioscience (Landmark. Print) 2022-04, Vol.27 (4), p.114 |
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| container_title | Frontiers in bioscience (Landmark. Print) |
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| creator | Banaszkiewicz, Marta Tarwacka, Paulina Krzywonos-Zawadzka, Anna Olejnik, Agnieszka Laprairie, Robert Noszczyk-Nowak, Agnieszka Sawicki, Grzegorz Bil-Lula, Iwona |
| description | Ischemia/reperfusion (I/R) is a pivotal mechanism of organ injury during clinical stetting for example for cardiopulmonary bypasses. The generation of reactive oxygen species (ROS) during I/R induces oxidative stress that promotes endothelial dysfunction, DNA dissociation and local inflammation. In turn, those processes induce cytokine release, resulting in damage to cellular structures and cell death. One of the major psychoactive compounds of
is delta-9-tetrahydrocannabinol (Δ9-THC), which is known as an anti-inflammatory mediator. Our research aimed to test if Δ9-THC may be protective in the treatment of cardiovascular system dysfunction arising from I/R heart injury.
Two experimental models were used: isolated rat hearts perfused with the Langendorff method and human cardiac myocytes (HCM) culture. Rat hearts and HCM underwent
/chemical
I/R protocol with/without Δ9-THC treatment. The following parameters were measured: cell metabolic activity, morphology changes, cell damage as lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS level, total antioxidant capacity (TAC) and heart hemodynamic parameters.
Δ9-THC protected the heart, as evidenced by the improved recovery of cardiac function (
0.05, N = 3-6). Cells subjected to I/R showed lower cytoplasmic LDH activity, and 10 μM Δ9-THC treatment reduced cell injury and increased LDH content (
= 0.019, N = 6-9). Morphology changes of HCM-spherical shape, vacuolisation of cytoplasm and swollen mitochondria-were inhibited due to Δ9-THC treatment. I/R condition affected cell viability, but 10 μM Δ9-THC decreased the number of dead cells (
= 0.005, N = 6-9). The total level of CERK was lower in the I/R group, reflecting oxidative/nitrosative stress changes. The administration of Δ9-THC effectively increased the production of CERK to the level of aerobic control (
= 0.028, N = 6-9). ROS level was significantly decreased in I/R cells (
= 0.007, N = 6-8), confirming oxidative stress, while administration of 10 μM Δ9-THC enhanced TAC in cardiomyocytes subjected to I/R (
= 0.010, N = 6-8).
Δ9-THC promotes the viability of cardiomyocytes, improves their metabolic activity, decreases cell damage and restores heart mechanical function, serving as a cardioprotective. We proposed the use of Δ9-THC as a cardioprotective drug to be, administered before onset of I/R protocol. |
| doi_str_mv | 10.31083/j.fbl2704114 |
| format | article |
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is delta-9-tetrahydrocannabinol (Δ9-THC), which is known as an anti-inflammatory mediator. Our research aimed to test if Δ9-THC may be protective in the treatment of cardiovascular system dysfunction arising from I/R heart injury.
Two experimental models were used: isolated rat hearts perfused with the Langendorff method and human cardiac myocytes (HCM) culture. Rat hearts and HCM underwent
/chemical
I/R protocol with/without Δ9-THC treatment. The following parameters were measured: cell metabolic activity, morphology changes, cell damage as lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS level, total antioxidant capacity (TAC) and heart hemodynamic parameters.
Δ9-THC protected the heart, as evidenced by the improved recovery of cardiac function (
0.05, N = 3-6). Cells subjected to I/R showed lower cytoplasmic LDH activity, and 10 μM Δ9-THC treatment reduced cell injury and increased LDH content (
= 0.019, N = 6-9). Morphology changes of HCM-spherical shape, vacuolisation of cytoplasm and swollen mitochondria-were inhibited due to Δ9-THC treatment. I/R condition affected cell viability, but 10 μM Δ9-THC decreased the number of dead cells (
= 0.005, N = 6-9). The total level of CERK was lower in the I/R group, reflecting oxidative/nitrosative stress changes. The administration of Δ9-THC effectively increased the production of CERK to the level of aerobic control (
= 0.028, N = 6-9). ROS level was significantly decreased in I/R cells (
= 0.007, N = 6-8), confirming oxidative stress, while administration of 10 μM Δ9-THC enhanced TAC in cardiomyocytes subjected to I/R (
= 0.010, N = 6-8).
Δ9-THC promotes the viability of cardiomyocytes, improves their metabolic activity, decreases cell damage and restores heart mechanical function, serving as a cardioprotective. We proposed the use of Δ9-THC as a cardioprotective drug to be, administered before onset of I/R protocol.</description><identifier>EISSN: 2768-6698</identifier><identifier>DOI: 10.31083/j.fbl2704114</identifier><identifier>PMID: 35468673</identifier><language>eng</language><publisher>Singapore</publisher><subject>Animals ; Antioxidants ; Cardiotonic Agents - pharmacology ; Dronabinol - pharmacology ; Dronabinol - therapeutic use ; Hallucinogens - pharmacology ; Rats ; Reactive Oxygen Species ; Reperfusion</subject><ispartof>Frontiers in bioscience (Landmark. Print), 2022-04, Vol.27 (4), p.114</ispartof><rights>2022 The Author(s). Published by IMR Press.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,870,27957,27958</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35468673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Banaszkiewicz, Marta</creatorcontrib><creatorcontrib>Tarwacka, Paulina</creatorcontrib><creatorcontrib>Krzywonos-Zawadzka, Anna</creatorcontrib><creatorcontrib>Olejnik, Agnieszka</creatorcontrib><creatorcontrib>Laprairie, Robert</creatorcontrib><creatorcontrib>Noszczyk-Nowak, Agnieszka</creatorcontrib><creatorcontrib>Sawicki, Grzegorz</creatorcontrib><creatorcontrib>Bil-Lula, Iwona</creatorcontrib><title>Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a Cardioprotective Agent in the Future Treatment</title><title>Frontiers in bioscience (Landmark. Print)</title><addtitle>Front Biosci (Landmark Ed)</addtitle><description>Ischemia/reperfusion (I/R) is a pivotal mechanism of organ injury during clinical stetting for example for cardiopulmonary bypasses. The generation of reactive oxygen species (ROS) during I/R induces oxidative stress that promotes endothelial dysfunction, DNA dissociation and local inflammation. In turn, those processes induce cytokine release, resulting in damage to cellular structures and cell death. One of the major psychoactive compounds of
is delta-9-tetrahydrocannabinol (Δ9-THC), which is known as an anti-inflammatory mediator. Our research aimed to test if Δ9-THC may be protective in the treatment of cardiovascular system dysfunction arising from I/R heart injury.
Two experimental models were used: isolated rat hearts perfused with the Langendorff method and human cardiac myocytes (HCM) culture. Rat hearts and HCM underwent
/chemical
I/R protocol with/without Δ9-THC treatment. The following parameters were measured: cell metabolic activity, morphology changes, cell damage as lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS level, total antioxidant capacity (TAC) and heart hemodynamic parameters.
Δ9-THC protected the heart, as evidenced by the improved recovery of cardiac function (
0.05, N = 3-6). Cells subjected to I/R showed lower cytoplasmic LDH activity, and 10 μM Δ9-THC treatment reduced cell injury and increased LDH content (
= 0.019, N = 6-9). Morphology changes of HCM-spherical shape, vacuolisation of cytoplasm and swollen mitochondria-were inhibited due to Δ9-THC treatment. I/R condition affected cell viability, but 10 μM Δ9-THC decreased the number of dead cells (
= 0.005, N = 6-9). The total level of CERK was lower in the I/R group, reflecting oxidative/nitrosative stress changes. The administration of Δ9-THC effectively increased the production of CERK to the level of aerobic control (
= 0.028, N = 6-9). ROS level was significantly decreased in I/R cells (
= 0.007, N = 6-8), confirming oxidative stress, while administration of 10 μM Δ9-THC enhanced TAC in cardiomyocytes subjected to I/R (
= 0.010, N = 6-8).
Δ9-THC promotes the viability of cardiomyocytes, improves their metabolic activity, decreases cell damage and restores heart mechanical function, serving as a cardioprotective. We proposed the use of Δ9-THC as a cardioprotective drug to be, administered before onset of I/R protocol.</description><subject>Animals</subject><subject>Antioxidants</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Dronabinol - pharmacology</subject><subject>Dronabinol - therapeutic use</subject><subject>Hallucinogens - pharmacology</subject><subject>Rats</subject><subject>Reactive Oxygen Species</subject><subject>Reperfusion</subject><issn>2768-6698</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNo1kM1Kw0AcxBdBbKk9epU96iHtfmV3cyzR2kJF0Houm-S_TUqzCZuN0Pfw5EP5TEasp4HfDAMzCN1QMuOUaD4_zGx2ZIoISsUFGjMldSRlokdo2nUHQghLKE1ifYVGPBZSS8XH6Ov7Eyc42kLwpjwVvsmNcyarXHPEd2dvld7jdd365gM6vO7yEurKzF-hBW_7rmocXoHxAT-cOtu7PPwS4wr8XO3LgN_AfwA2HTY4Nb6omqEowJAa6GIPLuDK4VACXvah94C3HkyoB36NLq05djA96wS9Lx-36SravDyt08UmaofZIbJaJYQzYQ1juS3yWOecEQIAwpBYKUZoQWUMVmZC85jEVlulC2WEETIuJJ-g27_ets9qKHatr2rjT7v_k_gPD-9qXg</recordid><startdate>20220401</startdate><enddate>20220401</enddate><creator>Banaszkiewicz, Marta</creator><creator>Tarwacka, Paulina</creator><creator>Krzywonos-Zawadzka, Anna</creator><creator>Olejnik, Agnieszka</creator><creator>Laprairie, Robert</creator><creator>Noszczyk-Nowak, Agnieszka</creator><creator>Sawicki, Grzegorz</creator><creator>Bil-Lula, Iwona</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20220401</creationdate><title>Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a Cardioprotective Agent in the Future Treatment</title><author>Banaszkiewicz, Marta ; Tarwacka, Paulina ; Krzywonos-Zawadzka, Anna ; Olejnik, Agnieszka ; Laprairie, Robert ; Noszczyk-Nowak, Agnieszka ; Sawicki, Grzegorz ; Bil-Lula, Iwona</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p108t-f8790324fa22cfdc58c3200eee4a0577201d165ef6b483505f8f78d7a4a465d63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Animals</topic><topic>Antioxidants</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Dronabinol - pharmacology</topic><topic>Dronabinol - therapeutic use</topic><topic>Hallucinogens - pharmacology</topic><topic>Rats</topic><topic>Reactive Oxygen Species</topic><topic>Reperfusion</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Banaszkiewicz, Marta</creatorcontrib><creatorcontrib>Tarwacka, Paulina</creatorcontrib><creatorcontrib>Krzywonos-Zawadzka, Anna</creatorcontrib><creatorcontrib>Olejnik, Agnieszka</creatorcontrib><creatorcontrib>Laprairie, Robert</creatorcontrib><creatorcontrib>Noszczyk-Nowak, Agnieszka</creatorcontrib><creatorcontrib>Sawicki, Grzegorz</creatorcontrib><creatorcontrib>Bil-Lula, Iwona</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Frontiers in bioscience (Landmark. Print)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Banaszkiewicz, Marta</au><au>Tarwacka, Paulina</au><au>Krzywonos-Zawadzka, Anna</au><au>Olejnik, Agnieszka</au><au>Laprairie, Robert</au><au>Noszczyk-Nowak, Agnieszka</au><au>Sawicki, Grzegorz</au><au>Bil-Lula, Iwona</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a Cardioprotective Agent in the Future Treatment</atitle><jtitle>Frontiers in bioscience (Landmark. Print)</jtitle><addtitle>Front Biosci (Landmark Ed)</addtitle><date>2022-04-01</date><risdate>2022</risdate><volume>27</volume><issue>4</issue><spage>114</spage><pages>114-</pages><eissn>2768-6698</eissn><abstract>Ischemia/reperfusion (I/R) is a pivotal mechanism of organ injury during clinical stetting for example for cardiopulmonary bypasses. The generation of reactive oxygen species (ROS) during I/R induces oxidative stress that promotes endothelial dysfunction, DNA dissociation and local inflammation. In turn, those processes induce cytokine release, resulting in damage to cellular structures and cell death. One of the major psychoactive compounds of
is delta-9-tetrahydrocannabinol (Δ9-THC), which is known as an anti-inflammatory mediator. Our research aimed to test if Δ9-THC may be protective in the treatment of cardiovascular system dysfunction arising from I/R heart injury.
Two experimental models were used: isolated rat hearts perfused with the Langendorff method and human cardiac myocytes (HCM) culture. Rat hearts and HCM underwent
/chemical
I/R protocol with/without Δ9-THC treatment. The following parameters were measured: cell metabolic activity, morphology changes, cell damage as lactate dehydrogenase (LDH) activity, ceramide kinase (CERK) activity, ROS level, total antioxidant capacity (TAC) and heart hemodynamic parameters.
Δ9-THC protected the heart, as evidenced by the improved recovery of cardiac function (
0.05, N = 3-6). Cells subjected to I/R showed lower cytoplasmic LDH activity, and 10 μM Δ9-THC treatment reduced cell injury and increased LDH content (
= 0.019, N = 6-9). Morphology changes of HCM-spherical shape, vacuolisation of cytoplasm and swollen mitochondria-were inhibited due to Δ9-THC treatment. I/R condition affected cell viability, but 10 μM Δ9-THC decreased the number of dead cells (
= 0.005, N = 6-9). The total level of CERK was lower in the I/R group, reflecting oxidative/nitrosative stress changes. The administration of Δ9-THC effectively increased the production of CERK to the level of aerobic control (
= 0.028, N = 6-9). ROS level was significantly decreased in I/R cells (
= 0.007, N = 6-8), confirming oxidative stress, while administration of 10 μM Δ9-THC enhanced TAC in cardiomyocytes subjected to I/R (
= 0.010, N = 6-8).
Δ9-THC promotes the viability of cardiomyocytes, improves their metabolic activity, decreases cell damage and restores heart mechanical function, serving as a cardioprotective. We proposed the use of Δ9-THC as a cardioprotective drug to be, administered before onset of I/R protocol.</abstract><cop>Singapore</cop><pmid>35468673</pmid><doi>10.31083/j.fbl2704114</doi><oa>free_for_read</oa></addata></record> |
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| identifier | EISSN: 2768-6698 |
| ispartof | Frontiers in bioscience (Landmark. Print), 2022-04, Vol.27 (4), p.114 |
| issn | 2768-6698 |
| language | eng |
| recordid | cdi_pubmed_primary_35468673 |
| source | DOAJ Directory of Open Access Journals |
| subjects | Animals Antioxidants Cardiotonic Agents - pharmacology Dronabinol - pharmacology Dronabinol - therapeutic use Hallucinogens - pharmacology Rats Reactive Oxygen Species Reperfusion |
| title | Δ 9 -Tetrahydrocannabinol (Δ 9 -THC) Improves Ischemia/Reperfusion Heart Dysfunction and Might Serve as a Cardioprotective Agent in the Future Treatment |
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