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The prophylactic and therapeutic effects of cannabidiol on lung injury secondary to cardiac ischemia model in rats via PERK/NRF2/CHOP/BCL2 pathway

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dc.creator Arlıoglu, Melih
dc.creator Milletsever, Adem
dc.creator İLHAN, İlter
dc.creator UYSAL, Dinçer
dc.creator AŞCI, Halil
dc.creator Ozmen, Ozlem
dc.creator Tasan, Serife
dc.creator Taner, Rumeysa
dc.date 2024-01-01T00:00:00Z
dc.date.accessioned 2025-02-25T10:19:16Z
dc.date.available 2025-02-25T10:19:16Z
dc.identifier 2da987af-6afc-4f6e-88a3-02cd0d980817
dc.identifier 10.1080/08923973.2024.2384904
dc.identifier https://avesis.sdu.edu.tr/publication/details/2da987af-6afc-4f6e-88a3-02cd0d980817/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/99207
dc.description Background: Inflammation and oxidative stress are key players in lung injury stemming from cardiac ischemia (LISCI). Cannabidiol (CBD) demonstrates tissue-protective properties through its antioxidant, anti-inflammatory, and anti-apoptotic characteristics. This study aims to assess the preventive (p-CBD) and therapeutic (t-CBD) effects of CBD on LISCI. Methods: Forty male Wistar Albino rats were divided into four groups: control (CON), LISCI, p-CBD, and t-CBD. The left anterior descending coronary artery was ligated for 30 min of ischemia followed by 30 min of reperfusion. Lung tissues were then extracted for histopathological, immunohistochemical, genetic, and biochemical analyses. Results: Histopathologically, marked hyperemia, increased septal tissue thickness, and inflammatory cell infiltrations were observed in the lung tissues of the LISCI group. Spectrophotometrically, total oxidant status and oxidative stress index levels were elevated, while total antioxidant status levels were decreased. Immunohistochemically, expressions of cyclooxygenase-1 (COX1), granulocyte colony-stimulating factor (GCSF), interleukin-6 (IL6) were increased. In genetic analyses, PERK and CHOP expressions were increased, whereas Nuclear factor erythroid 2-related factor 2 (NRF2) and B-cell leukemia/lymphoma 2 protein (BCL2) expressions were decreased. These parameters were alleviated by both prophylactic and therapeutic CBD treatment protocols. Conclusion: In LISCI-induced damage, both endoplasmic reticulum and mitochondrial stress, along with oxidative and inflammatory markers, were triggered, resulting in lung cell damage. However, both p-CBD and t-CBD treatments effectively reversed these mechanisms, normalizing all histopathological, biochemical, and PCR parameters.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title The prophylactic and therapeutic effects of cannabidiol on lung injury secondary to cardiac ischemia model in rats via PERK/NRF2/CHOP/BCL2 pathway
dc.type info:eu-repo/semantics/article


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