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Background <p>The risk of liver injury is increased by persistent hyperglycemia. Diabetes-related liver damage involves both oxidative stress and an abnormal inflammatory response. Nevertheless, many plants possess notable pharmaceutical properties, such as <i>Portulaca oleracea</i> (purslane, PE), which stands out for its wide range of potential medicinal applications globally. Consequently, this research sought to investigate the possibilities of purslane ethanolic extract in protecting against liver damage, oxidative stress, and the inflammatory response associated with diabetes.</p> Methods <p>Diabetes was induced in rats through a high-fat diet, followed by a single intraperitoneal injection of 35 mg/kg of streptozotocin (STZ). The diabetic rats were treated with PE at dose of (100 mg/kg), metformin (MT) at dose of (100 mg/kg) or combination therapy of (50 mg/kg) PE plus (50 mg/kg) MT for 4 weeks. Prooxidants (TBARS, XO, and NO) levels, antioxidant enzymes activity (SOD and GPx), inflammatory markers (TNF-α, IL-1β, and IFN-γ), and hepatic architecture abnormalities were measured by using standardized protocols.</p> Results <p>Rats treated with STZ exhibited notable elevations in tissue prooxidants (TBARS, XO, and NO), and inflammatory markers (TNF-α, IL-1β, and IFN-γ), with a parallel reduction in the activity of tissue antioxidants (SOD and GPx). Severe histopathological include vacuolated hepatocytes, dilated congested central veins, and numerous apoptotic signs, in addition to histochemical alterations in the liver tissue, were noted. When diabetic animals were treated with MT, PE ethanolic extract, or a combination of MT plus PE, these deleterious effects were improved.</p> Conclusion <p>All together the obtained data confirmed that PE displayed an ameliorating effect against the liver damage, inflammatory response, and oxidative damage linked to <i>diabetic mellitus.</i></p>

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Hepatic restorative potential of Portulaca oleracea ethanolic extract and/or metformin in type II diabetes mellitus model induced by high-fat diet and STZ

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月31日

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  • Naglaa Bahr,
  • Amna H. M. Nour,
  • Abd M. Abd El-KaderEl-Kader,
  • Maha A. El Demellawy,
  • Doaa A. Ghareeb

摘要

Background

The risk of liver injury is increased by persistent hyperglycemia. Diabetes-related liver damage involves both oxidative stress and an abnormal inflammatory response. Nevertheless, many plants possess notable pharmaceutical properties, such as Portulaca oleracea (purslane, PE), which stands out for its wide range of potential medicinal applications globally. Consequently, this research sought to investigate the possibilities of purslane ethanolic extract in protecting against liver damage, oxidative stress, and the inflammatory response associated with diabetes.

Methods

Diabetes was induced in rats through a high-fat diet, followed by a single intraperitoneal injection of 35 mg/kg of streptozotocin (STZ). The diabetic rats were treated with PE at dose of (100 mg/kg), metformin (MT) at dose of (100 mg/kg) or combination therapy of (50 mg/kg) PE plus (50 mg/kg) MT for 4 weeks. Prooxidants (TBARS, XO, and NO) levels, antioxidant enzymes activity (SOD and GPx), inflammatory markers (TNF-α, IL-1β, and IFN-γ), and hepatic architecture abnormalities were measured by using standardized protocols.

Results

Rats treated with STZ exhibited notable elevations in tissue prooxidants (TBARS, XO, and NO), and inflammatory markers (TNF-α, IL-1β, and IFN-γ), with a parallel reduction in the activity of tissue antioxidants (SOD and GPx). Severe histopathological include vacuolated hepatocytes, dilated congested central veins, and numerous apoptotic signs, in addition to histochemical alterations in the liver tissue, were noted. When diabetic animals were treated with MT, PE ethanolic extract, or a combination of MT plus PE, these deleterious effects were improved.

Conclusion

All together the obtained data confirmed that PE displayed an ameliorating effect against the liver damage, inflammatory response, and oxidative damage linked to diabetic mellitus.