Surgical neurology international · 2026
Effect of erythropoietin on serum brain-derived neurotrophic factor after experimental traumatic brain injury in Wistar rats: A randomized controlled laboratory study.
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Hasan Hasan, Suryaningtyas Wihasto, Parenrengi Muhammad Arifin, Wungu Citrawati Dyah Kencono
Аннотация
BACKGROUND: Traumatic brain injury (TBI) initiates secondary injury cascades that can reduce brain-derived neurotrophic factor (BDNF), a key mediator of synaptic plasticity and repair. Erythropoietin (EPO) has nonhematopoietic neuroprotective effects and may upregulate BDNF, while serum BDNF is a feasible translational pharmacodynamic biomarker. The aim of this study was to evaluate whether repeated intraperitoneal EPO administration increased serum BDNF levels on post-injury day 7 in Wistar rats with experimental TBI.
METHODS: Male Wistar rats (2.5-3 months; 200-250 g) were allocated to sham, TBI + normal saline, or TBI + EPO (5,000 IU/kg intraperitoneally at 1 h, 24 h, 48 h, and day 7). Focal unilateral TBI was induced using a weight-drop model under ketamine/xylazine anesthesia. Serum BDNF (ng/mL) was measured by enzyme-linked immunosorbent assay on day 7. Group differences were tested using one-way analysis of variance with Tukey post hoc testing (two-sided α = 0.05).
RESULTS: Analyzable samples were sham n = 10, TBI + saline n = 10, and TBI + EPO n = 9. Mean ± standard deviation serum BDNF was 0.336 ± 0.164, 0.288 ± 0.111, and 0.770 ± 0.170 ng/mL, respectively. Overall differences were significant (P < 0.001). EPO increased BDNF versus sham and saline (P < 0.001), while saline and sham did not differ (P = 1.000).
CONCLUSION: Repeated EPO dosing significantly increased serum BDNF 7 days after experimental TBI, supporting BDNF-linked neuroprotective signaling and the utility of serum BDNF as a pharmacodynamic biomarker. Dose- response, longer follow-up, and multimodal outcomes are required before clinical translation.
METHODS: Male Wistar rats (2.5-3 months; 200-250 g) were allocated to sham, TBI + normal saline, or TBI + EPO (5,000 IU/kg intraperitoneally at 1 h, 24 h, 48 h, and day 7). Focal unilateral TBI was induced using a weight-drop model under ketamine/xylazine anesthesia. Serum BDNF (ng/mL) was measured by enzyme-linked immunosorbent assay on day 7. Group differences were tested using one-way analysis of variance with Tukey post hoc testing (two-sided α = 0.05).
RESULTS: Analyzable samples were sham n = 10, TBI + saline n = 10, and TBI + EPO n = 9. Mean ± standard deviation serum BDNF was 0.336 ± 0.164, 0.288 ± 0.111, and 0.770 ± 0.170 ng/mL, respectively. Overall differences were significant (P < 0.001). EPO increased BDNF versus sham and saline (P < 0.001), while saline and sham did not differ (P = 1.000).
CONCLUSION: Repeated EPO dosing significantly increased serum BDNF 7 days after experimental TBI, supporting BDNF-linked neuroprotective signaling and the utility of serum BDNF as a pharmacodynamic biomarker. Dose- response, longer follow-up, and multimodal outcomes are required before clinical translation.