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Carvacrol exerts anti-inflammatory, anti-oxidative stress and hepatoprotective effects against diclofenac-induced liver injury in male rats
Molood Barzan1, Mahdi Heydari2, Hamzeh Mirshekari-Jahangiri3, Hassan Firouzi4, Maryam Dastan5, Mohammad Najafi6, Mansoor Khaledi7, Ali Nouri6, Mehran Ebrahimi Shah-abadi8
1 Department of Molecular Cell Biology and Microbiology, Islamic Azad University of Tehran, Tehran, Iran; Please note that following authors considered as first author: Molood Barzan and Mahdi Heydari, Iran
2 Department of Anatomical Sciences, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran; Please note that following authors considered as first author: Molood Barzan and Mahdi Heydari, Iran
3 Department of Physiology, Iran University of Medical Sciences, Tehran, Iran
4 Department of Medical Laboratory Science, Islamic Azad University, Sari Branch, Sari, Iran
5 Department of Physiology, Faculty of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran
6 Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran
7 Department of Microbiology, Faculty of Medicine, Shahed University, Tehran, Iran
8 Department of Surgery, Afzalipour Hospital, Kerman University of Medical Sciences, Kerman, Iran
Correspondence Address:
Ali Nouri
Department of Biochemistry, Faculty of Medicine, Iran University of Medical Sciences, Tehran
Iran
Mehran Ebrahimi Shah-abadi
Department of Surgery, Afzalipour Hospital, Kerman University of Medical Sciences, Kerman
Iran
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/ijpvm.ijpvm_178_21
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Background: Diclofenac (DIC) is an NSAID that can cause toxic effects in animals and humans and carvacrol (CAR) is a monoterpene compound that displays effective pharmacological and biological actions. The purpose of this work was to assess the influences of CAR on DIC-induced liver injury and oxidative stress in male rats. Methods: The male Wistar rats were segregated into four groups. Group 1, the control group; Group 2 received DIC-only (10 mg/kg BW, p.o); Group 3, received CAR-only (10 mg/kg BW, p.o), and group 4 received DIC plus CAR. The serum levels as well as the activity of several liver-associated markers, and oxidative and anti-oxidant compounds were tested. The expression of pro-inflammatory mediators was also studied using the qRT-PCR analysis. Results: Our results showed that DIC treatment was associated with the elevation in the serum levels of liver-related markers together with the increase in the serum and the hepatic levels of malondialdehyde (MDA) and protein carbonyl (PC). Moreover, DIC reduced the activity of the antioxidant system in the rats and increased lymphocyte infiltration into the hepatocytes. CAR; however, protected the hepatocytes from the toxic effects of DIC by enhancing the activity of antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and Glutathione (GSH). By diminishing the expression of tumor necrosis factor (TNF)-α, CAR was also capable of preventing the inflammatory effects of DIC on liver cells. Conclusions: The findings of this study indicated that the administration of CAR could alleviate the noxious effects of DIC on the antioxidant defense system and liver tissue.
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