Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury

Cadmium (Cd) is a toxic heavy metal that can cause severe hepatotoxicity in the body. This study investigates the hepatoprotective effects of Beta-Caryophyllene (BCP), a natural sesquiterpene, against Cd-induced liver injury. In the study, the protective effects of BCP on biological processes such a...

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Main Authors: Merve BOLAT, İsmail BOLAT, Samet TEKİN, Tuğçe YILMAZ
Format: Article
Language:English
Published: Kafkas University, Faculty of Veterinary Medicine 2025-08-01
Series:Kafkas Universitesi Veteriner Fakültesi Dergisi
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Online Access:https://vetdergikafkas.org/pdf.php?id=3212
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author Merve BOLAT
İsmail BOLAT
Samet TEKİN
Tuğçe YILMAZ
author_facet Merve BOLAT
İsmail BOLAT
Samet TEKİN
Tuğçe YILMAZ
author_sort Merve BOLAT
collection DOAJ
description Cadmium (Cd) is a toxic heavy metal that can cause severe hepatotoxicity in the body. This study investigates the hepatoprotective effects of Beta-Caryophyllene (BCP), a natural sesquiterpene, against Cd-induced liver injury. In the study, the protective effects of BCP on biological processes such as oxidative stress, inflammation and apoptosis were investigated through TLR4/NF-κB, SIRT1/KEAP1/Nrf2/HO-1 and Bax/ Bcl-2/Caspase3 signaling pathways. For this purpose, 50 male rats were divided into 5 groups: Control, Cd, BCP100+Cd, BCP200+Cd and BCP200, 10 in each group. At the end of the study, it was determined that Cd exposure caused damage to cells by increasing lipid peroxidation, oxidative stress and inflammation in liver tissue. However, BCP treatment was found to reduce oxidative damage by increasing antioxidant enzyme activities (SOD, GSH, CAT) and reducing lipid peroxidation (MDA). Furthermore, it was determined that BCP lowered proinflammatory cytokine levels (TNF-α, IL-1β) by inhibiting TLR4/NF-κB signaling activity, while also increasing anti-inflammatory IL- 10 levels. It was also observed that BCP inhibits the suppression of Nrf2 through KEAP1 by activating the Nrf2 signaling pathway, resulting in elevated levels of SIRT and HO-1. In the analyses of apoptosis, it was determined that BCP inhibited Caspase3 activity and reduced apoptosis in liver cells by balancing the Bax/Bcl-2 ratio. These findings suggest that BCP provides potent protection against Cd-induced liver toxicity by regulating various signaling pathways and could potentially be used as a hepatoprotective agent.
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spelling doaj-art-a665b695e5c446b4bae78aeed3debca82025-08-20T03:46:16ZengKafkas University, Faculty of Veterinary MedicineKafkas Universitesi Veteriner Fakültesi Dergisi1309-22512025-08-0131449750610.9775/kvfd.2025.341353212Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injuryMerve BOLAT0İsmail BOLAT1Samet TEKİN2Tuğçe YILMAZ3Department of Physiology, Faculty of Veterinary Medicine, Atatürk University, TR-25200 Erzurum - TÜRKİYEDepartment of Pathology, Faculty of Veterinary Medicine, Atatürk University, TR- 25200 Erzurum - TÜRKİYEDepartment of Physiology, Faculty of Veterinary Medicine, Atatürk University, TR-25200 Erzurum - TÜRKİYEDepartment of Pathology, Faculty of Veterinary Medicine, Atatürk University, TR- 25200 Erzurum - TÜRKİYECadmium (Cd) is a toxic heavy metal that can cause severe hepatotoxicity in the body. This study investigates the hepatoprotective effects of Beta-Caryophyllene (BCP), a natural sesquiterpene, against Cd-induced liver injury. In the study, the protective effects of BCP on biological processes such as oxidative stress, inflammation and apoptosis were investigated through TLR4/NF-κB, SIRT1/KEAP1/Nrf2/HO-1 and Bax/ Bcl-2/Caspase3 signaling pathways. For this purpose, 50 male rats were divided into 5 groups: Control, Cd, BCP100+Cd, BCP200+Cd and BCP200, 10 in each group. At the end of the study, it was determined that Cd exposure caused damage to cells by increasing lipid peroxidation, oxidative stress and inflammation in liver tissue. However, BCP treatment was found to reduce oxidative damage by increasing antioxidant enzyme activities (SOD, GSH, CAT) and reducing lipid peroxidation (MDA). Furthermore, it was determined that BCP lowered proinflammatory cytokine levels (TNF-α, IL-1β) by inhibiting TLR4/NF-κB signaling activity, while also increasing anti-inflammatory IL- 10 levels. It was also observed that BCP inhibits the suppression of Nrf2 through KEAP1 by activating the Nrf2 signaling pathway, resulting in elevated levels of SIRT and HO-1. In the analyses of apoptosis, it was determined that BCP inhibited Caspase3 activity and reduced apoptosis in liver cells by balancing the Bax/Bcl-2 ratio. These findings suggest that BCP provides potent protection against Cd-induced liver toxicity by regulating various signaling pathways and could potentially be used as a hepatoprotective agent.https://vetdergikafkas.org/pdf.php?id=3212apoptosisbeta caryophyllenecadmiumhepatotoxicityinflammationoxidative stress
spellingShingle Merve BOLAT
İsmail BOLAT
Samet TEKİN
Tuğçe YILMAZ
Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
Kafkas Universitesi Veteriner Fakültesi Dergisi
apoptosis
beta caryophyllene
cadmium
hepatotoxicity
inflammation
oxidative stress
title Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
title_full Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
title_fullStr Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
title_full_unstemmed Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
title_short Mechanistic insights into the mitigating role of beta-caryophyllene on cadmium-induced liver injury
title_sort mechanistic insights into the mitigating role of beta caryophyllene on cadmium induced liver injury
topic apoptosis
beta caryophyllene
cadmium
hepatotoxicity
inflammation
oxidative stress
url https://vetdergikafkas.org/pdf.php?id=3212
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AT ismailbolat mechanisticinsightsintothemitigatingroleofbetacaryophylleneoncadmiuminducedliverinjury
AT samettekin mechanisticinsightsintothemitigatingroleofbetacaryophylleneoncadmiuminducedliverinjury
AT tugceyilmaz mechanisticinsightsintothemitigatingroleofbetacaryophylleneoncadmiuminducedliverinjury