Hepatoprotective Effects of Dawa-Ul-Kurkum, a Unani Polyherbal Preparation and the Possible Mechanisms in Experimental Model of Ethanol Induced Liver Damage in Rats

Journal of pharmacy and pharmacology research Pub Date : 2022-01-01 DOI:10.26502/fjppr.057

Mohd Rafi Reshi, K. Gulati, M. Naqvi, Nafaa Hassan, A. Ray

{"title":"Hepatoprotective Effects of Dawa-Ul-Kurkum, a Unani Polyherbal Preparation and the Possible Mechanisms in Experimental Model of Ethanol Induced Liver Damage in Rats","authors":"Mohd Rafi Reshi, K. Gulati, M. Naqvi, Nafaa Hassan, A. Ray","doi":"10.26502/fjppr.057","DOIUrl":null,"url":null,"abstract":"The liver is an important organ that is involved in metabolism, storage, secretion, and detoxification. Chronic alcohol misuse can cause hepatotoxicity, putting the liver's normal function in jeopardy. Hepatotoxicity caused by ethanol is primarily caused by toxic byproducts of its metabolism, which cause oxidative stress [1]. Alcohol is a psychoactive chemical that has been linked to a variety of health concerns around the world [2]. Oxidative stress is one of the key mechanisms of ethanol-induced hepatotoxicity. Alcohol dehydrogenase converts ethanol to acetaldehyde, which is then oxidized to acetate by acetaldehyde dehydrogenase [3-6]. When ethanol is taken in excess, it is converted mostly to acetaldehyde by the enzyme cytochrome P450 (CYP2E1), which is implicated in the production of reactive oxygen species (ROS) [7-9]. As a result, oxidative stress is caused by an increase in ROS combined with a reduction in antioxidant capability. Recent research suggests that ethanol-induced oxidative stress plays a key role in the development and progression of alcoholic liver disease [10-12]. Abstract","PeriodicalId":73897,"journal":{"name":"Journal of pharmacy and pharmacology research","volume":"49 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of pharmacy and pharmacology research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.26502/fjppr.057","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}

引用次数: 2

Abstract

The liver is an important organ that is involved in metabolism, storage, secretion, and detoxification. Chronic alcohol misuse can cause hepatotoxicity, putting the liver's normal function in jeopardy. Hepatotoxicity caused by ethanol is primarily caused by toxic byproducts of its metabolism, which cause oxidative stress [1]. Alcohol is a psychoactive chemical that has been linked to a variety of health concerns around the world [2]. Oxidative stress is one of the key mechanisms of ethanol-induced hepatotoxicity. Alcohol dehydrogenase converts ethanol to acetaldehyde, which is then oxidized to acetate by acetaldehyde dehydrogenase [3-6]. When ethanol is taken in excess, it is converted mostly to acetaldehyde by the enzyme cytochrome P450 (CYP2E1), which is implicated in the production of reactive oxygen species (ROS) [7-9]. As a result, oxidative stress is caused by an increase in ROS combined with a reduction in antioxidant capability. Recent research suggests that ethanol-induced oxidative stress plays a key role in the development and progression of alcoholic liver disease [10-12]. Abstract

查看原文本刊更多论文

乌兰尼多药制剂达瓦乌尔库姆的保肝作用及其在乙醇诱导大鼠肝损伤实验模型中的可能机制

肝脏是参与代谢、储存、分泌和解毒的重要器官。长期酒精滥用会导致肝毒性，使肝脏的正常功能处于危险之中。乙醇引起的肝毒性主要是由其代谢的有毒副产物引起的，这些副产物引起氧化应激。酒精是一种精神活性化学物质，与世界各地的各种健康问题有关。氧化应激是乙醇肝毒性的重要机制之一。乙醇脱氢酶将乙醇转化为乙醛，然后乙醛脱氢酶将其氧化为乙酸[3-6]。当乙醇摄入过量时，它主要通过细胞色素P450 (CYP2E1)酶转化为乙醛，这与活性氧(ROS)的产生有关[7-9]。因此，氧化应激是由ROS的增加和抗氧化能力的降低引起的。最近的研究表明，乙醇诱导的氧化应激在酒精性肝病的发生和发展中起着关键作用[10-12]。摘要

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Journal of pharmacy and pharmacology research

自引率

0.00%

发文量