Published January 1, 2024 | Version v1
Journal article Open

Humanin's impact on pain markers and neuronal viability in diabetic neuropathy model

  • 1. Firat Univ, Sch Med, Dept Biophys, TR-23119 Elazig, Turkiye
  • 2. Gaziantep Islam Sci & Technol Univ, Sch Med, Dept Biophys, Gaziantep, Turkiye
  • 3. Firat Univ, Sch Med, Dept Physiol, Elazig, Turkiye
  • 4. Firat Univ, Sch Med, Dept Anaesthesiol & Reanimat, Elazig, Turkiye
  • 5. Univ Medipol, Sch Med, Dept Physiol, Istanbul, Turkiye
  • 6. Firat Univ, Sch Med, Dept Histol & Embryol, Elazig, Turkiye
  • 7. Univ Inonu, Sch Med, Dept Physiol, Malatya, Turkiye

Description

Objective This study investigates the impact of chronic humanin (HN) treatment on pain-related markers (NMDA, substance P, TRPV1, and IL-1 beta) in diabetic mice's dorsal root ganglia (DRG). Additionally, we assess the effects of HN on cellular viability in DRG neurons. Methods In vivo experiments involved 15 days of HN administration (4 mg/kg) to diabetic mice (n = 10). Protein levels of NMDA, IL-1 beta, TRPV1, and substance P were measured in diabetic DRG. In vitro experiments explored HN's impact on apoptosis and cellular viability, focusing on the JAK2/STAT3 pathway. Results Humanin significantly reduced the elevated expression of NMDA, IL-1 beta, TRPV1, and substance P induced by diabetes (p < .05). Furthermore, HN treatment increased cellular viability in DRG neurons through JAK2/STAT3 pathway activation (p < .05). Conclusion These findings highlight the significance of understanding mitochondrial function and pain markers, as well as apoptosis in diabetes. The study provides insights for managing the condition and its complications.

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