Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension
Cannabidiol (CBD) is a plant-derived compound with antioxidant and anti-inflammatory properties. Pulmonary hypertension (PH) is still an incurable disease. CBD has been suggested to ameliorate monocrotaline (MCT)-induced PH, including reduction in right ventricular systolic pressure (RVSP), a vasore...
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2022-05-01
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author | Anna Krzyżewska Marta Baranowska-Kuczko Anna Jastrząb Irena Kasacka Hanna Kozłowska |
author_facet | Anna Krzyżewska Marta Baranowska-Kuczko Anna Jastrząb Irena Kasacka Hanna Kozłowska |
author_sort | Anna Krzyżewska |
collection | DOAJ |
description | Cannabidiol (CBD) is a plant-derived compound with antioxidant and anti-inflammatory properties. Pulmonary hypertension (PH) is still an incurable disease. CBD has been suggested to ameliorate monocrotaline (MCT)-induced PH, including reduction in right ventricular systolic pressure (RVSP), a vasorelaxant effect on pulmonary arteries and a decrease in the white blood cell count. The aim of our study was to investigate the effect of chronic administration of CBD (10 mg/kg daily for 21 days) on the parameters of oxidative stress and inflammation in the lungs of rats with MCT-induced PH. In MCT-induced PH, we found a decrease in total antioxidant capacity (TAC) and glutathione level (GSH), an increase in inflammatory parameters, e.g., tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), nuclear factor kappa B (NF-κB), monocyte chemoattractant protein-1 (MCP-1), and cluster of differentiation 68 (CD68), and the overexpression of cannabinoid receptors type 1 and 2 (CB<sub>1</sub>-Rs, CB<sub>2</sub>-Rs). Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB<sub>1</sub>-Rs expression and levels of inflammatory mediators such as TNF-α, IL -1β, NF-κB, MCP-1 and CD68. In conclusion, CBD has antioxidant and anti-inflammatory effects in MCT-induced PH. CBD may act as an adjuvant therapy for PH, but further detailed preclinical and clinical studies are recommended to confirm our promising results. |
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spelling | doaj.art-b7f17727a5274495b62549b5000f31882023-11-23T12:24:41ZengMDPI AGMolecules1420-30492022-05-012710332710.3390/molecules27103327Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary HypertensionAnna Krzyżewska0Marta Baranowska-Kuczko1Anna Jastrząb2Irena Kasacka3Hanna Kozłowska4Department of Experimental Physiology and Pathophysiology, Medical University of Bialystok, Mickiewicz 2A, 15-222 Bialystok, PolandDepartment of Experimental Physiology and Pathophysiology, Medical University of Bialystok, Mickiewicz 2A, 15-222 Bialystok, PolandDepartment of Analytical Chemistry, Medical University of Bialystok, Mickiewicz 2D, 15-222 Bialystok, PolandDepartment of Histology and Cytophysiology, Medical University of Bialystok, Mickiewicz 2C, 15-222 Bialystok, PolandDepartment of Experimental Physiology and Pathophysiology, Medical University of Bialystok, Mickiewicz 2A, 15-222 Bialystok, PolandCannabidiol (CBD) is a plant-derived compound with antioxidant and anti-inflammatory properties. Pulmonary hypertension (PH) is still an incurable disease. CBD has been suggested to ameliorate monocrotaline (MCT)-induced PH, including reduction in right ventricular systolic pressure (RVSP), a vasorelaxant effect on pulmonary arteries and a decrease in the white blood cell count. The aim of our study was to investigate the effect of chronic administration of CBD (10 mg/kg daily for 21 days) on the parameters of oxidative stress and inflammation in the lungs of rats with MCT-induced PH. In MCT-induced PH, we found a decrease in total antioxidant capacity (TAC) and glutathione level (GSH), an increase in inflammatory parameters, e.g., tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), nuclear factor kappa B (NF-κB), monocyte chemoattractant protein-1 (MCP-1), and cluster of differentiation 68 (CD68), and the overexpression of cannabinoid receptors type 1 and 2 (CB<sub>1</sub>-Rs, CB<sub>2</sub>-Rs). Administration of CBD increased TAC and GSH concentrations, glutathione reductase (GSR) activity, and decreased CB<sub>1</sub>-Rs expression and levels of inflammatory mediators such as TNF-α, IL -1β, NF-κB, MCP-1 and CD68. In conclusion, CBD has antioxidant and anti-inflammatory effects in MCT-induced PH. CBD may act as an adjuvant therapy for PH, but further detailed preclinical and clinical studies are recommended to confirm our promising results.https://www.mdpi.com/1420-3049/27/10/3327pulmonary hypertensioncannabidioloxidative stressinflammationmonocrotaline |
spellingShingle | Anna Krzyżewska Marta Baranowska-Kuczko Anna Jastrząb Irena Kasacka Hanna Kozłowska Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension Molecules pulmonary hypertension cannabidiol oxidative stress inflammation monocrotaline |
title | Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension |
title_full | Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension |
title_fullStr | Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension |
title_full_unstemmed | Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension |
title_short | Cannabidiol Improves Antioxidant Capacity and Reduces Inflammation in the Lungs of Rats with Monocrotaline-Induced Pulmonary Hypertension |
title_sort | cannabidiol improves antioxidant capacity and reduces inflammation in the lungs of rats with monocrotaline induced pulmonary hypertension |
topic | pulmonary hypertension cannabidiol oxidative stress inflammation monocrotaline |
url | https://www.mdpi.com/1420-3049/27/10/3327 |
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