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

Abstract

Objective

This study investigates the impact of chronic humanin (HN) treatment on pain-related markers (NMDA, substance P, TRPV1, and IL-1β) 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-1β, 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-1β, 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.

Keywords:

• Humanin
• dorsal root ganglia
• pain markers
• apoptosis
• cell viability
• diabetic neuropathy

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

The datasets generated during and/or analysed during the current study are available from the corresponding author on reasonable request.

Additional information

Funding

This study was supported by Turkish Scientific Technical Research Organization (TUBITAK) under Project No.: 119R084.