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<p>Diabetic encephalopathy is a chronic neurodegenerative complication of diabetes mellitus characterized by cognitive decline, neuroinflammation, oxidative stress, and impaired insulin signaling. Semaglutide, a glucagon-like peptide-1 receptor agonist, has demonstrated neuroprotective potential; however, whether dietary antioxidant supplementation can provide additional neurobiological benefit remains unclear. This study investigated the neuroprotective effects of semaglutide alone and in combination with papaya fruit pulp in a streptozotocin-induced rat model of diabetic encephalopathy, with emphasis on oxidative stress, insulin signaling, neuroinflammation, amyloidogenesis, and neuronal integrity. Forty male rats were allocated into four groups: control, diabetic (STZ), diabetic treated with semaglutide (0.9&#xa0;mg/kg), and diabetic treated with semaglutide (0.3&#xa0;mg/kg) combined with 10% papaya juice for eight weeks. Notably, butyrylcholinesterase activity was normalized only in the semaglutide-papaya group, indicating a distinct cholinergic regulatory effect. Histological examination of the hippocampus and cerebral cortex confirmed superior preservation of neuronal architecture in the combination-treated animals. These findings indicate that while semaglutide mediates the primary metabolic, insulin-sensitizing, and anti-inflammatory effects, papaya provides a complementary neuroprotective contribution through selective reinforcement of antioxidant and cholinergic pathways. Rather than demonstrating global statistical synergy, the semaglutide-papaya combination exhibits pathway-specific enhancement, supporting a biologically meaningful combinatorial strategy for mitigating diabetic encephalopathy.</p>

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Complementary neuroprotective effects of semaglutide and papaya in diabetic encephalopathy via antioxidant and insulin-signaling pathways

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月6日

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  • Mohamed M. Zeweil,
  • Mai M. Ali,
  • Marium M. Shamaa,
  • Faten I. Mohammed,
  • Marwa Kamal,
  • Mohamed Samir Ahmed Zaki,
  • Afaf Alharthi,
  • Amera A. Ahmed,
  • Amr Elkelish,
  • Mohamed S. Abdel-Maksoud,
  • Komla Mawunyo Dossouvi,
  • Asmaa F. Khafaga

摘要

Diabetic encephalopathy is a chronic neurodegenerative complication of diabetes mellitus characterized by cognitive decline, neuroinflammation, oxidative stress, and impaired insulin signaling. Semaglutide, a glucagon-like peptide-1 receptor agonist, has demonstrated neuroprotective potential; however, whether dietary antioxidant supplementation can provide additional neurobiological benefit remains unclear. This study investigated the neuroprotective effects of semaglutide alone and in combination with papaya fruit pulp in a streptozotocin-induced rat model of diabetic encephalopathy, with emphasis on oxidative stress, insulin signaling, neuroinflammation, amyloidogenesis, and neuronal integrity. Forty male rats were allocated into four groups: control, diabetic (STZ), diabetic treated with semaglutide (0.9 mg/kg), and diabetic treated with semaglutide (0.3 mg/kg) combined with 10% papaya juice for eight weeks. Notably, butyrylcholinesterase activity was normalized only in the semaglutide-papaya group, indicating a distinct cholinergic regulatory effect. Histological examination of the hippocampus and cerebral cortex confirmed superior preservation of neuronal architecture in the combination-treated animals. These findings indicate that while semaglutide mediates the primary metabolic, insulin-sensitizing, and anti-inflammatory effects, papaya provides a complementary neuroprotective contribution through selective reinforcement of antioxidant and cholinergic pathways. Rather than demonstrating global statistical synergy, the semaglutide-papaya combination exhibits pathway-specific enhancement, supporting a biologically meaningful combinatorial strategy for mitigating diabetic encephalopathy.