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Clin Exp Emerg Med > Accepted Articles
doi: https://doi.org/10.15441/ceem.24.266    [Accepted]
The Long-term influences of Age-At-Injury on Neuroinflammation and neuronal Apoptosis following Traumatic Brain Injury in Pediatric and Adulthood Mice
Jin-Soo Park1, Hyun-Jeong Park2 , Young-Min Kim2 , Hyun-Seok Chai2 , Gwan Jin Park1,2 , Sang-Chul Kim1,2 , Gyeong-Gyu Yu2 , Suk-Woo Lee1,2 , Hoon Kim1,2
1Department of Emergency Medicine, Chungbuk National University Hospital, 776, Sunhwan-ro, Seowon-gu, Cheongju, Republic of Korea
2Department of Emergency Medicine, College of Medicine, Chungbuk National University, 1, Chungdae-ro, Seowon-gu, Cheongju, Republic of Korea
Correspondence  Hoon Kim Tel: + 82-43-261-2847, Fax: +82-43-269-7810, Email: nichekh2000@chungbuk.ac.kr
Received: June 6, 2024. Revised: September 7, 2024.  Accepted: November 7, 2024. Published online: January 14, 2025.
ABSTRACT
Objective
The study aims to investigate the long-term impacts of traumatic brain injury (TBI) on neuroinflammation and neuronal apoptosis in pediatric and adult mice, specifically focusing on how age-at-injury influences these processes..
Methods
Controlled cortical impact (CCI) was used to induce TBI in pediatric (21-25 days old) and adult (8-12 weeks old) C57Bl/6 male mice. Neuroinflammation was evaluated through immunoreactivity for Iba-1 and GFAP, while apoptosis was assessed using markers such as Bax, Bcl- 2, and pro-caspase-3. Additionally, HSP70 expression was measured to understand the stress response.
Result
s Following CCI, pediatric mice exhibited a significant reduction in NeuN expression(p < 0.001), significant increase in GFAP (p < 0.01) and AIF-1/Iba1 expression (p < 0.05) at 3 dpi compared to sham controls. In contrast, adult mice exhibited no significant change in AIF-1/Iba1 expression and a less pronounced increase in GFAP (p < 0.05) at 3 dpi compared to sham controls. Pediatric mice demonstrated a more significant increase in Bax/Bcl-2 ratio at 7 dpi (p < 0.01), While adult mice a little weak significant increase in Bax/Bcl-2 ratio at 7 dpi (p < 0.05). Both age groups showed a significant but transient increase in HSP70 levels at 7 dpi, which normalized by 90 dpi.
Conclusions
Pediatric and adult mice exhibited significant time-dependent differences in neuroinflammation and apoptosis following TBI, with pediatric mice showing more intense early responses, highlighting age-specific vulnerabilities in post-injury outcomes. Both age groups showed a significant but transient increase in HSP70 expression, suggesting an acute stress response postinjury.
Keywords: Age-at-Injury, Controlled cortical impact, Neuro-inflammation, Apoptosis, Heat shock protein 70, Neuroprotection
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