Treatment with Cannabidiol Results in an Antioxidant and Cardioprotective Effect in Several Pathophysiologies | Bentham Science
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Current Hypertension Reviews

Editor-in-Chief

ISSN (Print): 1573-4021
ISSN (Online): 1875-6506

Perspective

Treatment with Cannabidiol Results in an Antioxidant and Cardioprotective Effect in Several Pathophysiologies

Author(s): Natasha M.C. Oliveira, Dayane A. Machado, Thauann L. da Silva and Gabriel T. do Vale*

Volume 18, Issue 2, 2022

Published on: 21 September, 2022

Page: [125 - 129] Pages: 5

DOI: 10.2174/1573402118666220513164101

Open Access Journals Promotions 2
Abstract

Cannabis sativa has chemically active compounds called cannabinoids, where Δ9- tetrahydrocannabinol (THC) and Cannabidiol (CBD) are the major ones responsible for the various pharmacological effects. The endocannabinoid system is an endogenous system considered a unique and widespread homeostatic physiological regulator. It is made up of type 1 (CB1) and type 2 (CB2) cannabinoid receptors. CBD, in turn, has a low affinity for CB1 and CB2 receptors, and regulates the effects arising from THC as a CB1 partial agonist, which are tachycardia, anxiety, and sedation. It also acts as a CB2 inverse agonist, resulting in anti-inflammatory effects. Furthermore, its anticonvulsant, neuroprotective, antipsychotic, antiemetic, anxiolytic, anticancer, and antioxidant effects seem to be linked to other discovered receptors such as GRP55, 5TH1a, TRPV I, TRPV II and the regulation of the intracellular concentration of Ca2+. Regarding oxidative stress, O2- can act as an oxidizing agent, being reduced to hydrogen peroxide (H2O2), or as a reducing agent, donating its extra electron to NO to form peroxynitrite (ONOO-). The ONOO- formed is capable of oxidizing proteins, lipids, and nucleic acids, causing several cell damages. In this sense, CBD can prevent cardiac oxidative damage in many conditions, such as hypertension, diabetes, or even through the cardiotoxic effects induced by chemotherapy, which makes it a potential target for future clinical use to minimize the deleterious effects of many pathophysiologies.

Keywords: Cannabidiol, oxidative stress, heart, cardiotoxicity, antioxidant, pathophyriologies.

Graphical Abstract
[1]
Ebbert JO, Scharf EL, Hurt RT. Medical cannabis. Mayo Clin Proc 2018; 93(12): 1842-7.
[http://dx.doi.org/10.1016/j.mayocp.2018.09.005] [PMID: 30522595]
[2]
Di Marzo V, Piscitelli F. The endocannabinoid system and its modulation by phytocannabinoids. Neurotherapeutics 2015; 12(4): 692-8.
[http://dx.doi.org/10.1007/s13311-015-0374-6] [PMID: 26271952]
[3]
Fouad AA, Albuali WH, Al-Mulhim AS, Jresat I. Cardioprotective effect of cannabidiol in rats exposed to doxorubicin toxicity. Environ Toxicol Pharmacol 2013; 36(2): 347-57.
[http://dx.doi.org/10.1016/j.etap.2013.04.018] [PMID: 23721741]
[4]
Britch SC, Babalonis S, Walsh SL. Cannabidiol: Pharmacology and therapeutic targets. Psychopharmacology 2021; 238(1): 9-28.
[http://dx.doi.org/10.1007/s00213-020-05712-8] [PMID: 33221931]
[5]
Remiszewski P, Jarocka-Karpowicz I, Biernacki M, et al. Chronic cannabidiol administration fails to diminish blood pressure in rats with primary and secondary hypertension despite its effects on cardiac and plasma endocannabinoid system, oxidative stress and lipid metabolism. Int J Mol Sci 2020; 21(4): 1295.
[http://dx.doi.org/10.3390/ijms21041295] [PMID: 32075117]
[6]
Atalay S, Jarocka-Karpowicz I, Skrzydlewska E. Antioxidative and anti-inflammatory properties of cannabidiol. Antioxidants 2019; 9(1): 21.
[http://dx.doi.org/10.3390/antiox9010021] [PMID: 31881765]
[7]
Santos CX, Anilkumar N, Zhang M, Brewer AC, Shah AM. Redox signaling in cardiac myocytes. Free Radic Biol Med 2011; 50(7): 777-93.
[http://dx.doi.org/10.1016/j.freeradbiomed.2011.01.003] [PMID: 21236334]
[8]
Tan Y, Li X, Prabhu SD, Brittian KR, Chen Q, Yin X, et al. Angiotensin II plays a critical role in alcohol-induced cardiac nitrative damage, cell death, remodeling, and cardiomyopathy in a PKC/NADPH oxidase-dependent manner. J Am Coll Cardiol 2012; 59(16): 1477-86.
[http://dx.doi.org/10.1016/j.jacc.2011.12.034] [PMID: 22497828]
[9]
Touyz RM, Schiffrin EL. Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells. Pharmacol Rev 2000; 52(4): 639-72.
[PMID: 11121512]
[10]
Babior BM. NADPH oxidase. Curr Opin Immunol 2004; 16(1): 42-7.
[http://dx.doi.org/10.1016/j.coi.2003.12.001] [PMID: 14734109]
[11]
Paravicini TM, Touyz RM. NADPH oxidases, reactive oxygen species, and hypertension: Clinical implications and therapeutic possibilities. Diabetes Care 2008; 31 (Suppl. 2): S170-80.
[http://dx.doi.org/10.2337/dc08-s247] [PMID: 18227481]
[12]
Sumimoto H. Structure, regulation and evolution of Nox-family NADPH oxidases that produce reactive oxygen species. FEBS J 2008; 275(13): 3249-77.
[http://dx.doi.org/10.1111/j.1742-4658.2008.06488.x] [PMID: 18513324]
[13]
Beckman JS, Koppenol WH. Nitric oxide, superoxide, and peroxynitrite: The good, the bad, and ugly. Am J Physiol 1996; 271(5 Pt 1): C1424-37.
[http://dx.doi.org/10.1152/ajpcell.1996.271.5.C1424] [PMID: 8944624]
[14]
Gongora MC, Qin Z, Laude K, et al. Role of extracellular superoxide dismutase in hypertension. Hypertension 2006; 48(3): 473-81.
[http://dx.doi.org/10.1161/01.HYP.0000235682.47673.ab] [PMID: 16864745]
[15]
Tajima M, Kurashima Y, Sugiyama K, Ogura T, Sakagami H. The redox state of glutathione regulates the hypoxic induction of HIF-1. Eur J Pharmacol 2009; 606(1-3): 45-9.
[http://dx.doi.org/10.1016/j.ejphar.2009.01.026] [PMID: 19374849]
[16]
Ceron CS, Rizzi E, Guimarães DA, Martins-Oliveira A, Gerlach RF, Tanus-Santos JE. Nebivolol attenuates prooxidant and profibrotic mechanisms involving TGF-β and MMPs, and decreases vascular remodeling in renovascular hypertension. Free Radic Biol Med 2013; 65: 47-56.
[http://dx.doi.org/10.1016/j.freeradbiomed.2013.06.033] [PMID: 23806385]
[17]
Husain K, Vazquez-Ortiz M, Lalla J. Down regulation of aortic nitric oxide and antioxidant systems in chronic alcohol-induced hypertension in rats. Hum Exp Toxicol 2007; 26(5): 427-34.
[http://dx.doi.org/10.1177/0960327106072993] [PMID: 17623767]
[18]
Singh K, Kaur J, Ahluwalia P, Sharma J. Effect of monosodium glutamate on various lipid fractions and certain antioxidant enzymes in arterial tissue of chronic alcoholic adult male mice. Toxicol Int 2012; 19(1): 9-14.
[http://dx.doi.org/10.4103/0971-6580.94507] [PMID: 22736896]
[19]
Hao E, Mukhopadhyay P, Cao Z, et al. Cannabidiol protects against doxorubicin-induced cardiomyopathy by modulating mitochondrial function and biogenesis. Mol Med 2015; 21(1): 38-45.
[http://dx.doi.org/10.2119/molmed.2014.00261] [PMID: 25569804]
[20]
García-Martín A, Navarrete C, Garrido-Rodríguez M, et al. EHP-101 alleviates angiotensin II-induced fibrosis and inflammation in mice. Biomed Pharmacother 2021; 142: 112007.
[http://dx.doi.org/10.1016/j.biopha.2021.112007] [PMID: 34385107]
[21]
Matouk AI, Taye A, El-Moselhy MA, Heeba GH, Abdel-Rahman AA. Abnormal cannabidiol confers cardioprotection in diabetic rats independent of glycemic control. Eur J Pharmacol 2018; 820: 256-64.
[http://dx.doi.org/10.1016/j.ejphar.2017.12.039] [PMID: 29274332]
[22]
Fouda MA, Ghovanloo MR, Ruben PC. Cannabidiol protects against high glucose-induced oxidative stress and cytotoxicity in cardiac voltage-gated sodium channels. Br J Pharmacol 2020; 177(13): 2932-46.
[http://dx.doi.org/10.1111/bph.15020] [PMID: 32077098]
[23]
Rajesh M, Mukhopadhyay P, Bátkai S, et al. Cannabidiol attenuates cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy. J Am Coll Cardiol 2010; 56(25): 2115-25.
[http://dx.doi.org/10.1016/j.jacc.2010.07.033] [PMID: 21144973]
[24]
Lee WS, Erdelyi K, Matyas C, et al. Cannabidiol limits t cell-mediated chronic autoimmune myocarditis: Implications to autoimmune disorders and organ transplantation. Mol Med 2016; 22(1): 136-46.
[http://dx.doi.org/10.2119/molmed.2016.00007] [PMID: 26772776]

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