Scholarlink

Background <p>Liver fibrosis represents a critical stage in the progression of chronic liver diseases and remains a major global health concern due to its potential to advance to cirrhosis and hepatic failure. Epigallocatechin-3-gallate (EGCG), the principal catechin in green tea, has demonstrated potent antioxidant and antifibrotic properties. However, its dose-dependent hepatoprotective efficacy and mechanism of action against chemically induced liver fibrosis remain insufficiently elucidated. This study aimed to evaluate the hepatoprotective effects and underlying mechanisms of EGCG at varying doses against thioacetamide (TAA)-induced hepatic fibrosis in rats.</p> Methods <p>Forty-two adult male rats were randomly divided into six groups (<i>n</i> = 7 per group): control, TAA, TAA + EGCG (50, 100, or 200&#xa0;mg/kg/day), and TAA + silibinin (100&#xa0;mg/kg/day). Liver fibrosis was induced by intraperitoneal injection of TAA (200&#xa0;mg/kg) three times per week for three weeks. EGCG and Silibinin were administered orally for the same duration. At experiment end, blood samples were collected for hematological and biochemical analysis, while liver tissues were examined histopathologically and assessed for oxidative stress biomarkers including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH).</p> Results <p>TAA administration caused marked hepatic injury characterized by significant increases in serum liver enzymes, bilirubin, white blood cells, and platelets, along with decreases in red blood cell indices, total protein, and albumin. Oxidative stress markers showed elevated MDA and reduced SOD and GSH levels. EGCG treatment significantly ameliorated these alterations in a dose-dependent manner, with the 200&#xa0;mg/kg dose producing effects comparable to Silibinin. Histopathological findings confirmed that EGCG mitigated fibrotic changes and preserved hepatic architecture.</p> Conclusion <p>EGCG exerts potent hepatoprotective and antifibrotic effects against TAA-induced hepatic fibrosis by enhancing antioxidant defense mechanisms and improving liver function. These findings highlight EGCG as a promising natural therapeutic candidate for preventing and managing liver fibrosis.</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

Effects of epigallocatechin-3-gallate against thioacetamide-induced liver fibrosis in rats

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年6月24日

查看全文
  • Zaenah Zuhair Alamri

摘要

Background

Liver fibrosis represents a critical stage in the progression of chronic liver diseases and remains a major global health concern due to its potential to advance to cirrhosis and hepatic failure. Epigallocatechin-3-gallate (EGCG), the principal catechin in green tea, has demonstrated potent antioxidant and antifibrotic properties. However, its dose-dependent hepatoprotective efficacy and mechanism of action against chemically induced liver fibrosis remain insufficiently elucidated. This study aimed to evaluate the hepatoprotective effects and underlying mechanisms of EGCG at varying doses against thioacetamide (TAA)-induced hepatic fibrosis in rats.

Methods

Forty-two adult male rats were randomly divided into six groups (n = 7 per group): control, TAA, TAA + EGCG (50, 100, or 200 mg/kg/day), and TAA + silibinin (100 mg/kg/day). Liver fibrosis was induced by intraperitoneal injection of TAA (200 mg/kg) three times per week for three weeks. EGCG and Silibinin were administered orally for the same duration. At experiment end, blood samples were collected for hematological and biochemical analysis, while liver tissues were examined histopathologically and assessed for oxidative stress biomarkers including malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione (GSH).

Results

TAA administration caused marked hepatic injury characterized by significant increases in serum liver enzymes, bilirubin, white blood cells, and platelets, along with decreases in red blood cell indices, total protein, and albumin. Oxidative stress markers showed elevated MDA and reduced SOD and GSH levels. EGCG treatment significantly ameliorated these alterations in a dose-dependent manner, with the 200 mg/kg dose producing effects comparable to Silibinin. Histopathological findings confirmed that EGCG mitigated fibrotic changes and preserved hepatic architecture.

Conclusion

EGCG exerts potent hepatoprotective and antifibrotic effects against TAA-induced hepatic fibrosis by enhancing antioxidant defense mechanisms and improving liver function. These findings highlight EGCG as a promising natural therapeutic candidate for preventing and managing liver fibrosis.