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CC BY 4.0 · Indian Journal of Neurotrauma 2025; 22(02): 134-137
DOI: 10.1055/s-0044-1782611
Original Article

Prolidase Enzyme Activity as a Potential Biomarker for Blast-Induced Traumatic Brain Injury: A Study in a Rat Model

Authors

  • Rahul Gupta 

    1   Department of Neurosurgery, National Institute of Mental Health and Neuro-Sciences, Bengaluru, Karnataka, India

  • Dhananjaya I. Bhat    *

    2   Department of Neurosurgery, Aster RV Hospital, Bengaluru, Karnataka, India

  • Dhaval Shukla 

    1   Department of Neurosurgery, National Institute of Mental Health and Neuro-Sciences, Bengaluru, Karnataka, India

  • Sarada Subramanian

    3   Department of Neurochemistry, National Institute of Mental Health and Neuro-Sciences, Bengaluru, Karnataka, India

  • Puru Bansal

    4   Department of Neurosurgery, Bansal's Arogya Hospital, Thane, Maharashtra, India

  • Geethu Krishna

    3   Department of Neurochemistry, National Institute of Mental Health and Neuro-Sciences, Bengaluru, Karnataka, India

  • Mini Jayan

    5   Department of Statistics, Christ University, Bengaluru, Karnataka, India

  • Bhagavatula Indira Devi    *

    1   Department of Neurosurgery, National Institute of Mental Health and Neuro-Sciences, Bengaluru, Karnataka, India

Funding None.
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Abstract

Blast-induced traumatic brain injury (TBI) poses a significant threat to individuals exposed to explosive events. We hypothesized that blast-induced neurotrauma is an oxidative stress to brain and hence prolidase (PD) enzyme, which is an antioxidant is recommended; its serum levels are better markers of degree of injury in the acute phase for TBI in a rat blast injury model. Results revealed that PD enzyme activity in the hippocampus showed a slight increase across high, medium, and low blast pressures, but remained lower than the sham group. However, serum PD enzyme activity levels were significantly higher in the blast-exposed groups compared to the sham group. Tau protein levels were significantly elevated in the blast-exposed groups. Longitudinal analysis demonstrated a decline in hippocampal PD activity over time, while tau protein levels progressively increased, suggesting a shift from initial oxidative stress to neurodegeneration. These findings suggest that blast injury triggers oxidative stress and subsequent neurodegenerative processes. The correlation with tau protein levels further supports the involvement of oxidative stress in neurodegeneration. In conclusion, this study provides insights into the underlying pathophysiological mechanisms of blast-induced TBI and highlights the potential utility of PD enzyme activity as a diagnostic marker.

Keywords

animal model - blast-induced-traumatic brain injury - neurodegeneration - oxidative stress - prolidase

Note

Work discussed in this article was presented in the award paper category at NTSI conference Jaipur August 2023.


* Authors contributed equally to this work.




Publikationsverlauf

Artikel online veröffentlicht:
29. April 2024

© 2024. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/)

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