The long-term influences of age at injury on neuroinflammation and neuronal apoptosis following traumatic brain injury in pediatric and adult mice
- Author:
Jin-Soo PARK
1
;
Hyun-Jeong PARK
;
Young-Min KIM
;
Hyun-Seok CHAI
;
Gwan Jin PARK
;
Sang-Chul KIM
;
Gyeong-Gyu YU
;
Suk-Woo LEE
;
Hoon KIM
Author Information
- Publication Type:Original Article
- From: Clinical and Experimental Emergency Medicine 2025;12(3):267-279
- CountryRepublic of Korea
- Language:English
-
Abstract:
Objective:The study explores the long-term impacts of traumatic brain injury (TBI) on neuroinflammation and neuronal apoptosis in pediatric and adult mice, focusing on how age at injury influences these processes.
Methods:Controlled cortical impacts were used to induce TBI in pediatric (21–25 days old) and adult (8–12 weeks old) C57BL/6 male mice. Neuroinflammation was evaluated by measuring immunoreactivity for allograft inflammatory factor 1 (AIF-1)/ionized calcium-binding adaptor molecule 1 (Iba-1) and glial fibrillary acidic protein (GFAP), while apoptosis was assessed using markers such as B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, and procaspase-3. Additionally, heat shock protein 70 (HSP70) expression was measured to understand the stress response.
Results:Following controlled cortical impacts, pediatric mice exhibited a significant reduction in expression of neuronal nuclei (P<0.001), and significant increases in expression of GFAP (P<0.01) and AIF-1/Iba-1 (P<0.05) at 3 days post-injury (DPI) compared with sham controls. In contrast, adult mice exhibited no significant change in AIF-1/Iba-1 expression and a less pronounced increase in GFAP (P<0.05) at 3 DPI compared with sham controls. A more significant increase in Bax/Bcl-2 ratio at 7 DPI (P<0.01) was seen in pediatric mice, while a weak but significant increase in Bax/Bcl-2 ratio at 7 DPI (P<0.05) was evident in adults. Both age groups showed a significant but transient increase in HSP70 levels at 7 DPI, which normalized by 90 DPI.
Conclusion:Pediatric and adult mice exhibited significant time-dependent differences in neuroinflammation and apoptosis following TBI, with pediatric mice showing more intense early responses indicative of age-specific vulnerabilities in post-injury outcomes. Both age groups showed a significant but transient increase in HSP70 expression, suggesting an acute response to stress post-injury.
