Hasnaa Mansour, Marwa El-Zeftawy, M. Aboubakr, Rabab R Elzoghby
{"title":"n-乙酰半胱氨酸减轻四氯化碳所致大鼠急性肝损伤","authors":"Hasnaa Mansour, Marwa El-Zeftawy, M. Aboubakr, Rabab R Elzoghby","doi":"10.21608/nvvj.2022.152184.1007","DOIUrl":null,"url":null,"abstract":"The liver is a vital organ that performs most of the body's metabolic and detoxifying functions. There are various exogenous and endogenous factors that might cause liver issues. Carbon tetrachloride (CCL 4 ) 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 NAC has a protective effect in cases of liver injury or not. 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) CCL 4 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 CCL 4 via refinement tumor necrosis factor-alpha, interleukin-6 and reduced glutathione pathway.","PeriodicalId":210463,"journal":{"name":"New Valley Veterinary Journal","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"2022-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"N-Acetyl cysteine alleviates carbon-tetrachloride induced acute liver injury in rats\",\"authors\":\"Hasnaa Mansour, Marwa El-Zeftawy, M. Aboubakr, Rabab R Elzoghby\",\"doi\":\"10.21608/nvvj.2022.152184.1007\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"The liver is a vital organ that performs most of the body's metabolic and detoxifying functions. There are various exogenous and endogenous factors that might cause liver issues. Carbon tetrachloride (CCL 4 ) 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 NAC has a protective effect in cases of liver injury or not. 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) CCL 4 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 CCL 4 via refinement tumor necrosis factor-alpha, interleukin-6 and reduced glutathione pathway.\",\"PeriodicalId\":210463,\"journal\":{\"name\":\"New Valley Veterinary Journal\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-08-11\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"New Valley Veterinary Journal\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.21608/nvvj.2022.152184.1007\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"New Valley Veterinary Journal","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.21608/nvvj.2022.152184.1007","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
N-Acetyl cysteine alleviates carbon-tetrachloride induced acute liver injury in rats
The liver is a vital organ that performs most of the body's metabolic and detoxifying functions. There are various exogenous and endogenous factors that might cause liver issues. Carbon tetrachloride (CCL 4 ) 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 NAC has a protective effect in cases of liver injury or not. 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) CCL 4 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 CCL 4 via refinement tumor necrosis factor-alpha, interleukin-6 and reduced glutathione pathway.