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<p>Cisplatin (CP) is an effective platinum-based chemotherapeutic agent that is used to treat several types of cancer. CP administration is associated with several side effects including acute lung injury (ALI) and neurotoxicity. This study aimed at exploring the toxic impact of CP on the disruption of the lung–brain axis in rats and the protective role of curcumin (CUR) through examining a panel of blood-based biomarkers. CUR was administered at doses of 50 and 100 mg/kg/day for 14 days; interrupted by two intraperitoneal doses of CP (7 mg/kg body weight) on the 7th and the 14th days of the experimental period. Biochemical and histopathological investigations and serum levels of iron, Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), and nerve growth factor (NGF) were estimated. In addition, pulmonary and brain malondialdehyde (MDA), nitric oxide (NO), and catalase (CAT) were measured. CP caused significant elevation in lipid peroxidation and NO release, along with NLRP3 activation. In contrast, CAT activity, iron, and NGF levels were significantly reduced. Treatment of CP-induced rats with CUR 100 demonstrated higher protective activities than CUR 50. CUR exerted its protective potential against CP-induced pulmonary injury and neurotoxicity through alleviating oxidative damage and inflammation.</p>

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Protective impact of curcumin against cisplatin-induced central neurotoxicity and acute lung injury

  • 期刊论文

  • 发表日期：

    2026年4月23日

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  • Ghadha Ibrahim Fouad,
  • Hanan F. Aly,
  • Maha Z. Rizk

摘要

Cisplatin (CP) is an effective platinum-based chemotherapeutic agent that is used to treat several types of cancer. CP administration is associated with several side effects including acute lung injury (ALI) and neurotoxicity. This study aimed at exploring the toxic impact of CP on the disruption of the lung–brain axis in rats and the protective role of curcumin (CUR) through examining a panel of blood-based biomarkers. CUR was administered at doses of 50 and 100 mg/kg/day for 14 days; interrupted by two intraperitoneal doses of CP (7 mg/kg body weight) on the 7th and the 14th days of the experimental period. Biochemical and histopathological investigations and serum levels of iron, Nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3), and nerve growth factor (NGF) were estimated. In addition, pulmonary and brain malondialdehyde (MDA), nitric oxide (NO), and catalase (CAT) were measured. CP caused significant elevation in lipid peroxidation and NO release, along with NLRP3 activation. In contrast, CAT activity, iron, and NGF levels were significantly reduced. Treatment of CP-induced rats with CUR 100 demonstrated higher protective activities than CUR 50. CUR exerted its protective potential against CP-induced pulmonary injury and neurotoxicity through alleviating oxidative damage and inflammation.