N-Acetyl cysteine alleviates carbon-tetrachloride induced acute liver injury in rats | ||||
New Valley Veterinary Journal | ||||
Article 1, Volume 2, Issue 2, June 2022, Page 1-9 PDF (480.92 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/nvvj.2022.152184.1007 | ||||
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Authors | ||||
Hasnaa Mansour1; Marwa El-Zeftawy 2; Mohamed Aboubakr3; Rabab Elzoghby1 | ||||
1Pharmacology Department, Faculty of Veterinary Medicine, New Valley University, New Valley, Egypt | ||||
2Biochemistry Department, Faculty of Veterinary Medicine, New Valley University, New Valley, Egypt | ||||
3Pharmacology Department, Faculty of Veterinary Medicine, Benha University, 13736 Moshtohor, Toukh, Qaliobiya, Egypt. | ||||
Abstract | ||||
The liver is a vital organ that performs the majority of the body's metabolic and detoxifying functions. There are various exogenous and endogenous factors that might cause liver issues. Carbon tetrachloride (CCL4) is non-inflammable colorless organic compound and employed in a variety of industrial fields. N-acetylcysteine (NAC) is one of the prospective pharmaceutical candidates possesses multiple clinical applications. The purpose of this study is to determine whether or not NAC has a protective effect in cases of liver injury. Thirty male albino rats were involved in the study, which lasted one month. They were categorized into three groups: control, liver injury group (0.5 ml/kg rat body weight (Bwt) CCL4 administered orally twice a week), and protective group (150 mg/kg Bwt NAC supplied orally). Serum lipid and protein profiles and liver enzymes activities were evaluated. Antioxidant, oxidative stress and anti-inflammatory parameters were also assessed. Additionally, hepatic tissue was subjected to a histopathological investigation. The biochemical and histopathological results revealed dramatic improvement of studied parameters in NAC protective group comparing to liver injury one. Hence, we can conclude that, NAC shown a great potential in attenuating liver injury induced by CCL4 via refinement tumor necrosis factor-alpha, interleukin-6 and reduced glutathione pathway. | ||||
Keywords | ||||
Liver injury; Carbon tetrachloride; N-acetylcysteine; Oxidative stress, Inflammatory markers | ||||
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