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<p>Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac and aceclofenac are widely used for pain and inflammation but are major contributors to drug-induced liver injury (DILI), largely mediated through oxidative stress and hepatocellular damage. Identifying suitable experimental models and effective protective interventions is therefore essential. In this study, we employed the silkworm <i>Bombyx mori</i>, whose fat body displays functional similarities to the mammalian liver, to investigate NSAID-induced toxicity and evaluate potential ameliorative strategies. Following exposure to diclofenac and aceclofenac, silkworms exhibited a marked reduction in antioxidant enzyme activities and increased lipid peroxidation (LPO), along with elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), and phenol oxidase activity, confirming oxidative stress and tissue injury. Post-treatment with biosynthesized cerium oxide nanoparticles (CeO₂ NPs) partially restored antioxidant defenses and reduced LPO in a dose-dependent manner, consistent with their reactive oxygen species (ROS)-scavenging properties. However, CeO₂ NPs did not prevent ALT and AST elevation or normalize phenol oxidase (PO) activity, indicating limited protection against hepatocellular injury. In contrast, N-acetylcysteine (NAC), a clinically validated antioxidant, consistently preserved antioxidant enzyme activity, prevented LPO, and completely abrogated ALT, AST, and PO alterations. Collectively, these findings establish <i>B. mori</i> as a robust invertebrate model for studying NSAID-induced oxidative stress and tissue injury, reproducing key oxidative and injury-associated biomarker trends reported in mammalian systems. Furthermore, while NAC demonstrated superior protective efficacy, the antioxidant activity of CeO₂ NPs highlights their potential as emerging redox modulators, warranting further optimization and investigation in drug-induced toxicity.</p>

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Non-Steroidal Anti-Inflammatory Drugs-Induced Tissue Injury Modeled in an Invertebrate Model Organism Bombyx Mori and Ameliorative Potential of CeO2 Nanoparticle

  • 期刊论文

  • 发表日期：

    2026年3月21日

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  • Hashim Ashraf,
  • Sk Najrul Islam,
  • Nikhil Maheshvari,
  • Mariam Ahmad,
  • Absar Ahmad,
  • Ayesha Qamar

摘要

Non-steroidal anti-inflammatory drugs (NSAIDs) such as diclofenac and aceclofenac are widely used for pain and inflammation but are major contributors to drug-induced liver injury (DILI), largely mediated through oxidative stress and hepatocellular damage. Identifying suitable experimental models and effective protective interventions is therefore essential. In this study, we employed the silkworm Bombyx mori, whose fat body displays functional similarities to the mammalian liver, to investigate NSAID-induced toxicity and evaluate potential ameliorative strategies. Following exposure to diclofenac and aceclofenac, silkworms exhibited a marked reduction in antioxidant enzyme activities and increased lipid peroxidation (LPO), along with elevated alanine aminotransferase (ALT), aspartate aminotransferase (AST), and phenol oxidase activity, confirming oxidative stress and tissue injury. Post-treatment with biosynthesized cerium oxide nanoparticles (CeO₂ NPs) partially restored antioxidant defenses and reduced LPO in a dose-dependent manner, consistent with their reactive oxygen species (ROS)-scavenging properties. However, CeO₂ NPs did not prevent ALT and AST elevation or normalize phenol oxidase (PO) activity, indicating limited protection against hepatocellular injury. In contrast, N-acetylcysteine (NAC), a clinically validated antioxidant, consistently preserved antioxidant enzyme activity, prevented LPO, and completely abrogated ALT, AST, and PO alterations. Collectively, these findings establish B. mori as a robust invertebrate model for studying NSAID-induced oxidative stress and tissue injury, reproducing key oxidative and injury-associated biomarker trends reported in mammalian systems. Furthermore, while NAC demonstrated superior protective efficacy, the antioxidant activity of CeO₂ NPs highlights their potential as emerging redox modulators, warranting further optimization and investigation in drug-induced toxicity.