Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats
Carbon tetrachloride (CCl4) is a classic chemical hepatotoxicant that triggers liver damage through hepatic exacerbation of oxidative stress. Geraniol (GRL) is a natural bioactive acyclic monoterpene with several pharmacological effects. We thus explored whether GRL could prevent CCl4-triggered hepa...
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| Format: | Article |
| Language: | English |
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Elsevier
2024-06-01
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| Series: | Toxicology Reports |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S2214750024000076 |
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| author | Abdulmohsen I. Algefare Manal Alfwuaires Ademola C. Famurewa Hany Elsawy Azza Sedky |
| author_facet | Abdulmohsen I. Algefare Manal Alfwuaires Ademola C. Famurewa Hany Elsawy Azza Sedky |
| author_sort | Abdulmohsen I. Algefare |
| collection | DOAJ |
| description | Carbon tetrachloride (CCl4) is a classic chemical hepatotoxicant that triggers liver damage through hepatic exacerbation of oxidative stress. Geraniol (GRL) is a natural bioactive acyclic monoterpene with several pharmacological effects. We thus explored whether GRL could prevent CCl4-triggered hepatic toxicity. Rats were divided and administered GRL (100 mg/kg) and/or CCl4 (1 ml/kg of 1:1 v/v CCl4: olive oil) in Control group, GRL group, CCl4 group, GRL + CCl4 groups 2 times per week for 4 consecutive weeks. CCl4 caused significantly (p < 0.05) elevated serum activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (TB), whereas the albumin (ALB) and total protein (TP) levels were significantly (p < 0.05) reduced relative to the control group. The liver activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) decreased significantly (p < 0.05), while malondialdehyde (MDA) level evidently elevated in comparison to the control group. The CCl4 exposure caused significant increases in proinflammatory interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), apoptotic caspase-3 and caspase-9 levels, whereas the anti-inflammatory interleukin-4 (IL-4) and interleukin-10 (IL-10) were reduced in consistent with histopathological changes compared to the control. On the contrary, the GRL administration prevented the hepatic toxicity and lesions through restoration of liver status markers, antioxidant enzyme activities, MDA, cytokines and apoptosis in comparison to the CCl4 group. Altogether, the findings reveal that GRL could abrogate CCl4-provoked hepatic toxicity via inhibition of hepatic oxidative stress, inflammation and apoptosis in rats. |
| first_indexed | 2024-03-08T12:52:09Z |
| format | Article |
| id | doaj.art-34a599afa1084abea545fd4afe409de6 |
| institution | Directory Open Access Journal |
| issn | 2214-7500 |
| language | English |
| last_indexed | 2024-03-08T12:52:09Z |
| publishDate | 2024-06-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Toxicology Reports |
| spelling | doaj.art-34a599afa1084abea545fd4afe409de62024-01-20T04:45:37ZengElsevierToxicology Reports2214-75002024-06-0112128134Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in ratsAbdulmohsen I. Algefare0Manal Alfwuaires1Ademola C. Famurewa2Hany Elsawy3Azza Sedky4Department of Biological Sciences, College of Science, King Faisal University, Al-Ahsa 31982, Saudi ArabiaDepartment of Biological Sciences, College of Science, King Faisal University, Al-Ahsa 31982, Saudi ArabiaDepartment of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria; Department of Pharmacology, Manipal College of Pharmaceutical Sciences, Manipal Academy of Higher Education, Manipal, Karnataka State, India; Corresponding author at: Department of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University, Ndufu-Alike, Ikwo, Ebonyi State, Nigeria.Department of Chemistry, Faculty of Science, Tanta University, Tanta 31527, EgyptDepartment of Biological Sciences, College of Science, King Faisal University, Al-Ahsa 31982, Saudi Arabia; Department of Zoology, Faculty of Science, Alexandria University, Alexandria, Egypt; Correspondence to: Department of Biological Sciences, College of Science, King Faisal University, PO Box 400 Al-Ahsa, 31982 Al-Ahsa, Saudi Arabia.Carbon tetrachloride (CCl4) is a classic chemical hepatotoxicant that triggers liver damage through hepatic exacerbation of oxidative stress. Geraniol (GRL) is a natural bioactive acyclic monoterpene with several pharmacological effects. We thus explored whether GRL could prevent CCl4-triggered hepatic toxicity. Rats were divided and administered GRL (100 mg/kg) and/or CCl4 (1 ml/kg of 1:1 v/v CCl4: olive oil) in Control group, GRL group, CCl4 group, GRL + CCl4 groups 2 times per week for 4 consecutive weeks. CCl4 caused significantly (p < 0.05) elevated serum activities of alkaline phosphatase (ALP), aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (TB), whereas the albumin (ALB) and total protein (TP) levels were significantly (p < 0.05) reduced relative to the control group. The liver activities of catalase (CAT), glutathione peroxidase (GPx), and superoxide dismutase (SOD) decreased significantly (p < 0.05), while malondialdehyde (MDA) level evidently elevated in comparison to the control group. The CCl4 exposure caused significant increases in proinflammatory interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α), apoptotic caspase-3 and caspase-9 levels, whereas the anti-inflammatory interleukin-4 (IL-4) and interleukin-10 (IL-10) were reduced in consistent with histopathological changes compared to the control. On the contrary, the GRL administration prevented the hepatic toxicity and lesions through restoration of liver status markers, antioxidant enzyme activities, MDA, cytokines and apoptosis in comparison to the CCl4 group. Altogether, the findings reveal that GRL could abrogate CCl4-provoked hepatic toxicity via inhibition of hepatic oxidative stress, inflammation and apoptosis in rats.http://www.sciencedirect.com/science/article/pii/S2214750024000076GeraniolOxidative stressHepatotoxicantApoptosisHepatotoxicity |
| spellingShingle | Abdulmohsen I. Algefare Manal Alfwuaires Ademola C. Famurewa Hany Elsawy Azza Sedky Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats Toxicology Reports Geraniol Oxidative stress Hepatotoxicant Apoptosis Hepatotoxicity |
| title | Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats |
| title_full | Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats |
| title_fullStr | Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats |
| title_full_unstemmed | Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats |
| title_short | Geraniol prevents CCl4-induced hepatotoxicity via suppression of hepatic oxidative stress, pro-inflammation and apoptosis in rats |
| title_sort | geraniol prevents ccl4 induced hepatotoxicity via suppression of hepatic oxidative stress pro inflammation and apoptosis in rats |
| topic | Geraniol Oxidative stress Hepatotoxicant Apoptosis Hepatotoxicity |
| url | http://www.sciencedirect.com/science/article/pii/S2214750024000076 |
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