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Volume 18, Issue 3 (July 2024)                   IJT 2024, 18(3): 144-151 | Back to browse issues page

Ethics code: IR.LUMS.REC.1402.185


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Esmaeili A, Astaraki P, Jamalian M, Mohammadi H, Ziyaeenia N R. Protective Effect of Carvacrol Against Acute Liver Damage and Encephalopathy Induced by Thioacetamide. IJT 2024; 18 (3) :144-151
URL: http://ijt.arakmu.ac.ir/article-1-1320-en.html
1- Pharmacy Student, Student Research Committee, Lorestan University of Medical Sciences. Khoram-Abad, Iran.
2- Department of Internal Medicine, School of Medicine, Shahid Rahimi Hospital, Lorestan University of Medical Sciences, Khoram-Abad, Iran.
3- Department of Forensic Medicine, School of Medicine, Valiasr Hospital, Arak University of Medical Sciences, Arak, Iran.
4- Department of Toxicology, Faculty of Pharmacy, Razi Herbal Medicine Research Center, Lorestan University of Medical Sciences, Khoram-Abad, Iran. , hamidrezamohammadi65@yahoo.com
5- Department of Health Education, School of Medicine, Lorestan University of Medical Sciences, Khoram-Abad, Iran
Abstract:   (154 Views)
Background: Cancer occurs in 83% of liver diseases. Other risk factors for liver cancer include viral hepatitis, alcohol consumption, industrial chemicals, and a number of toxins. Another major disease that occurs following liver damage is hepatic encephalopathy. This condition arises primarily due to increased blood ammonia levels. Carvacrol, with antioxidant properties, reduces oxidative stress on the liver. The aim of this study was to investigate the effect of carvacrol on the improvement of hepatic encephalopathy in rats.
Methods: In this experimental study, 60 male Wistar rats were randomly divided into six groups of 10 each. Liver damage and induction of oxidative stress were caused in the rats by administering thioacetamide (100 mg/kg/day) intraperitoneally for three consecutive days. Carvacrol was administered by gavage at 25, 50, or 100 mg/kg/day after thioacetamide treatment. We investigated the biomarkers of liver damage in the blood, such as alanine transaminase, lactate dehydrogenase, total protein, and bilirubin. We also assessed the effect of oxidative stress, as the key inducer of hepatic encephalopathy, on the liver by measuring the lipid peroxidation, antioxidants, reactive oxygen species, glutathione reserves, and ammonium levels in the serum and brain.
Results: Thioacetamide significantly increased the biochemical markers in the rat sera, reflecting ammonium release and the development of oxidative stress (P<0.05). Conversely, the various doses of carvacrol significantly reduced the levels of biomarkers that are indicative of liver damage (P<0.05).
Conclusion: The study findings provided experimental evidence in favor of the therapeutic effects of carvacrol and against liver injury induced by thioacetamide, leading to encephalopathy.
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Type of Study: Research | Subject: General

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