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<p>Cisplatin (CP), a potent chemotherapeutic agent, is widely used in cancer treatment but often causes nephrotoxicity, leading to acute kidney injury (AKI). Oxidative stress and renal fibrosis are key contributors to CP-induced kidney damage, necessitating effective strategies to mitigate these adverse effects. Thiol-based antioxidants, such as 2-mercaptoethanol (2-BME), have shown promise in addressing oxidative stress and improving cellular resilience. In this study, 21 Wistar rats were divided into three groups: control, CP-treated, and CP + 2-BME-treated. CP-induced nephrotoxicity was modeled using a single intraperitoneal dose of CP (5&#xa0;mg/kg), while 2-BME was administered at 30&#xa0;mg/kg. Renal function was evaluated through blood urea nitrogen (BUN) and creatinine levels, and histopathological and immunohistochemical analyses assessed structural changes and fibrosis. CPbadministration caused significant renal damage, evidenced by elevated BUN and creatinine levels, tubular dilation, inflammatory infiltration, and increased fibrosis as marked by collagen deposition and α-SMA expression. Co-administration of 2-BME effectively ameliorated these effects by reducing, fibrosis markers, and renal injury scores, while restoring kidney function parameters to near-normal levels. 2-BME exhibits significant renoprotective effects against CP-induced nephrotoxicity through its antioxidant, anti-inflammatory, and anti-fibrotic properties. These findings highlight the potential of 2-BME as a therapeutic agent for mitigating renal injury in patients undergoing CP-based chemotherapy.</p>

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Protective effects of 2-mercaptoethanol on cisplatin-induced kidney injury in rats

  • 期刊论文

  • 发表日期：

    2025年8月28日

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  • Siamak Yari,
  • Bahar Mahmoodi

摘要

Cisplatin (CP), a potent chemotherapeutic agent, is widely used in cancer treatment but often causes nephrotoxicity, leading to acute kidney injury (AKI). Oxidative stress and renal fibrosis are key contributors to CP-induced kidney damage, necessitating effective strategies to mitigate these adverse effects. Thiol-based antioxidants, such as 2-mercaptoethanol (2-BME), have shown promise in addressing oxidative stress and improving cellular resilience. In this study, 21 Wistar rats were divided into three groups: control, CP-treated, and CP + 2-BME-treated. CP-induced nephrotoxicity was modeled using a single intraperitoneal dose of CP (5 mg/kg), while 2-BME was administered at 30 mg/kg. Renal function was evaluated through blood urea nitrogen (BUN) and creatinine levels, and histopathological and immunohistochemical analyses assessed structural changes and fibrosis. CPbadministration caused significant renal damage, evidenced by elevated BUN and creatinine levels, tubular dilation, inflammatory infiltration, and increased fibrosis as marked by collagen deposition and α-SMA expression. Co-administration of 2-BME effectively ameliorated these effects by reducing, fibrosis markers, and renal injury scores, while restoring kidney function parameters to near-normal levels. 2-BME exhibits significant renoprotective effects against CP-induced nephrotoxicity through its antioxidant, anti-inflammatory, and anti-fibrotic properties. These findings highlight the potential of 2-BME as a therapeutic agent for mitigating renal injury in patients undergoing CP-based chemotherapy.