Scholarlink

<p>It has been demonstrated that bile duct ligation (BDL) leads to an increase in free radical activity in the liver tissue. Free radicals interfere with hepatocytes and cause liver damage. Melatonin (Mel) and naringenin (NG) are two well-known antioxidants. In the present study, the effects of Mel and NG on liver damage induced by BDL were investigated. Eighteen Sprague–Dawley rats were divided into three groups: sham, BDL, and BDL + Mel and NG. Two weeks after BDL, animals received NG (daily) and Mel (every other day). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, and albumin levels were determined in order to assess hepatic function. Histological, immunohistological, and ultrastructural examinations were also performed to determine hepatic injury. AST, ALT, and MDA levels were elevated in the BDL group compared with the sham group, whereas this elevation was markedly decreased by Mel + NG treatment. Morphological assessment depicted normal liver parenchyma in the sham group and disorganization of hepatic cords, degeneration of hepatocytes, and proliferation of bile ducts within the portal area in the BDL group. These results demonstrated that administration of Mel + NG might lead to antioxidative effects against BDL-induced liver damage. As a result, it seems likely that treatment with Mel + NG has potential therapeutic value in protecting the liver against oxidative injury due to BDL.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Demonstration of the protective effects of melatonin and naringenin against hepatic injury induced by bile duct ligation in male rats

  • 期刊论文

  • 发表日期：

    2026年1月28日

查看全文
  • Majid Asadi-Shekaari,
  • Shahriar Dabiri,
  • Marzieh Maneshian,
  • Leila Jafaripour

摘要

It has been demonstrated that bile duct ligation (BDL) leads to an increase in free radical activity in the liver tissue. Free radicals interfere with hepatocytes and cause liver damage. Melatonin (Mel) and naringenin (NG) are two well-known antioxidants. In the present study, the effects of Mel and NG on liver damage induced by BDL were investigated. Eighteen Sprague–Dawley rats were divided into three groups: sham, BDL, and BDL + Mel and NG. Two weeks after BDL, animals received NG (daily) and Mel (every other day). Aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, and albumin levels were determined in order to assess hepatic function. Histological, immunohistological, and ultrastructural examinations were also performed to determine hepatic injury. AST, ALT, and MDA levels were elevated in the BDL group compared with the sham group, whereas this elevation was markedly decreased by Mel + NG treatment. Morphological assessment depicted normal liver parenchyma in the sham group and disorganization of hepatic cords, degeneration of hepatocytes, and proliferation of bile ducts within the portal area in the BDL group. These results demonstrated that administration of Mel + NG might lead to antioxidative effects against BDL-induced liver damage. As a result, it seems likely that treatment with Mel + NG has potential therapeutic value in protecting the liver against oxidative injury due to BDL.