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Dergiler / Maltepe Tıp Dergisi / 2025 / Cilt: 17 Sayı: 3

Deneysel Travmatik Beyin Hasarı Modelinde Serum İnterlökin-1 Beta’nın Zaman İçindeki Değişimi

Temporal Dynamics of Serum Interleukin-1 Beta Following Experimental Traumatic Brain Injury in Rats

Ozan Başkurt(ISTANBUL AREL UNIVERSITY, SCHOOL OF MEDICINE)0000-0003-1021-6529
Ece Uysal(ACIBADEM UNIVERSITY)0000-0002-2355-8395
İdris Avcı(USKUDAR UNIVERSITY)0000-0002-0378-9356
Selim Seker(ISTINYE UNIVERSITY)0000-0001-6939-6689
Hidayet Safak Cine(ISTANBUL MEDENIYET UNIVERSITY)0000-0002-0808-5921
Salih Batuhan Kartal(Bilge Hospital)0000-0002-8786-2492
Ege Coşkun(ISTANBUL AREL UNIVERSITY)0000-0002-5582-9786
Sayfa
66–71
Yayın Tarihi
2025-12-31
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Bulgular: Sham grubunda serum IL-1β iki fazlı bir eğilim gösterdi: 6. saatte başlangıçta düşüş, 72. saatte ise kısmi toparlanma.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Amaç: Travmatik beyin hasarı (TBI), sekonder nöronal hasarın temel aracısı olarak tanımlanan interlökin-1 beta’nın (IL-1β) rol aldığı karmaşık inflamatuvar kaskadları tetikler.
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Temel Bulgular & Veri:IL-1β’nin nöroenflamasyondaki rolü iyi bilinmesine rağmen, periferik dolaşımdaki dinamik profili yeterince karakterize edilmemiştir.
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Sonuç & Katkı:Bulgular: Sham grubunda serum IL-1β iki fazlı bir eğilim gösterdi: 6. saatte başlangıçta düşüş, 72. saatte ise kısmi toparlanma.
🔬Tür:Modelleme & Sayısal Simülasyon
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Biyomarker · IL-1β · Nöroenflamasyon

Özet

Amaç: Travmatik beyin hasarı (TBI), sekonder nöronal hasarın temel aracısı olarak tanımlanan interlökin-1 beta’nın (IL-1β) rol aldığı karmaşık inflamatuvar kaskadları tetikler. IL-1β’nin nöroenflamasyondaki rolü iyi bilinmesine rağmen, periferik dolaşımdaki dinamik profili yeterince karakterize edilmemiştir. Bu çalışmada, sıçanlarda deneysel TBI sonrası belirli zaman aralıklarında serum IL-1β düzeylerinin değerlendirilmesi ve bu biyobelirtecin potansiyelinin ve terapötik öneminin araştırılması amaçlanmıştır. Gereç ve Yöntemler: Toplam 40 erişkin erkek Sprague-Dawley sıçan rastgele beş gruba (n=8/grup) ayrıldı: bir sham grubu ve travmadan sonra 1, 6, 24 ve 72. saatlere karşılık gelen dört travma grubu. TBI, Marmarou ağırlık düşürme modeli ile oluşturuldu. Serum IL-1β konsantrasyonları ELISA yöntemi ile ölçüldü ve istatistiksel karşılaştırmalar tek yönlü ANOVA ve Tukey post-hoc testi ile yapıldı. Bulgular: Sham grubunda serum IL-1β iki fazlı bir eğilim gösterdi: 6. saatte başlangıçta düşüş, 72. saatte ise kısmi toparlanma. Travma grubunda ise dinamik bir patern izlendi: IL-1β 6. saatte azaldı (p=0.0356), 24. saatte anlamlı düzeyde zirve yaptı (p=0.0004, 6. saat ile karşılaştırıldığında) ve 72. saatte tekrar azaldı. Gruplar arası karşılaştırmalarda, travma grubunda 24. saatte IL-1β düzeylerinin sham grubuna göre anlamlı şekilde yüksek olduğu saptandı (p=0.0157). Sonuç: Bulgularımız, TBI sonrası serum IL-1β’nın zamana bağlı düzenlenmiş bir ekspresyon paterni sergilediğini ve 24. saatteki zirvenin terapötik hedefleme için potansiyel bir pencere olabileceğini göstermektedir. IL-1β, post-travmatik inflamasyonun izlenmesinde minimal invaziv bir biyobelirteç olarak kullanılabilir, ancak fonksiyonel sonuçlar ve santral doku düzeyleri ile korelasyonunun daha ileri araştırılması gerekmektedir.

Abstract

Aim: Traumatic brain injury (TBI) triggers complex inflammatory cascades, with interleukin-1 beta (IL-1β) identified as a key mediator of secondary neuronal damage. Although the role of IL-1β in neuroinflammation is well recognized, its dynamic profile in the peripheral circulation remains insufficiently characterized. This study aimed to assess serum IL-1β levels at defined intervals following experimental TBI in rats to elucidate its biomarker potential and therapeutic relevance. Material and Methods: A total of 40 adult male Sprague-Dawley rats were randomly allocated into five groups (n=8/group): one sham group and four trauma groups corresponding to 1, 6, 24, and 72 hours post-injury. TBI was induced using the Marmarou weight-drop model. Serum IL-1β concentrations were measured by ELISA, and statistical comparisons were made using one-way ANOVA with Tukey’s post hoc test. Results: In the sham group, serum IL-1β showed a biphasic trend: an initial decrease at 6 hours, followed by partial recovery by 72 hours. In contrast, the trauma group exhibited a dynamic pattern: IL-1β decreased at 6 hours (p=0.0356), peaked significantly at 24 hours (p=0.0004 vs. 6h), and declined again by 72 hours. Between-group comparisons revealed significantly elevated IL-1β levels in the trauma group at 24 hours (p=0.0157) compared to sham. Conclusion: Our findings suggest that serum IL-1β exhibits a temporally regulated expression pattern after TBI, with a peak at 24 hours representing a potential window for therapeutic targeting. IL-1β may serve as a minimally invasive biomarker to monitor post-traumatic inflammation, although correlation with functional outcomes and central tissue levels warrants further investigation.

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Bu Makaleye Atıf Yap

Başkurt, O., Uysal, E., Avcı, İ., Seker, S., Cine, H. S., Kartal, S. B., Coşkun, E. (2025). Deneysel Travmatik Beyin Hasarı Modelinde Serum İnterlökin-1 Beta’nın Zaman İçindeki Değişimi. Maltepe Tıp Dergisi, Cilt: 17 Sayı: 3, 66–71. https://doi.org/10.35514/mtd.2025.131

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Kaynakça (30)

  1. Referans 1 Mortezaee K, Khanlarkhani N, Beyer C, Zendedel A. Inflammasome: Its role in traumatic brain and spinal cord injury. J Cell Physiol. 2018 Jul;233(7):5160–9.
  2. Referans 2 Dekosky ST, Styren SD, O’Malley ME, Goss JR, Kochanek P, Marion D, et al. Interleukin-1 receptor antagonist suppresses neurotrophin response in injured rat brain. Ann Neurol. 1996;39(1):123–7.
  3. Referans 3 Lu K-T, Wu C-Y, Yen H-H, Peng J-HF, Wang C-L, Yang Y-L. Bumetanide administration attenuated traumatic brain injury through IL-1 overexpression. Neurol Res. 2007 Jun;29(4):404–9.
  4. Referans 4 Raghupathi R, McIntosh TK, Smith DH. Cellular responses to experimental brain injury. Brain Pathol. 1995 Oct;5(4):437–42.
  5. Referans 5 Samatra DPGP, Pratiwi NMD, Widyadharma IPE. High IL-1β serum as a predictor of decreased cognitive function in mild traumatic brain injury patients. Open Access Maced J Med Sci. 2018;6(9):1674–7.
  6. Referans 6 Fan L, Young PR, Barone FC, Feuerstein GZ, Smith DH, McIntosh TK. Experimental brain injury induces expression of interleukin-1 beta mRNA in the rat brain. Brain Res Mol Brain Res. 1995 May;30(1):125–30.
  7. Referans 7 Kuwar R, Rolfe A, Di L, Xu H, He L, Jiang Y, et al. A novel small molecular NLRP3 inflammasome inhibitor alleviates neuroinflammatory response following traumatic brain injury. J Neuroinflammation. 2019 Apr;16(1):81.
  8. Referans 8 Seplovich G, Bouchi Y, de Rivero Vaccari JP, Pareja JCM, Reisner A, Blackwell L, et al. Inflammasome links traumatic brain injury, chronic traumatic encephalopathy, and Alzheimer’s disease. Neural Regen Res. 2025 Jun;20(6):1644–64.
  9. Referans 9 Hao S, Yuan S, Liu Z, Hou B, Feng S, Zhang D. Neuroprotective effects of takinib on an experimental traumatic brain injury rat model via inhibition of transforming growth factor beta-activated kinase 1. Heliyon [Internet]. 2024;10(8):e29484. Available from: https://doi.org/10.1016/j.heliyon.2024.e29484.
  10. Referans 10 Zhou Z, Li Y, Peng R, Shi M, Gao W, Lei P, et al. Progesterone induces neuroprotection associated with immune/inflammatory modulation in experimental traumatic brain injury. Neuroreport. 2024 Apr;35(6):352–60.
  11. Referans 11 Marmarou A, Abd-Elfattah Foda MA, Van den Brink W, Campbell J, Kita H, Demetriadou K. A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. J Neurosurg. 1994;80(2):291–300.
  12. Referans 12 Abd-Elfattah Foda MA, Marmarou A. A new model of diffuse brain injury in rats. Part II: Morphological characterization. J Neurosurg. 1994;80(2):301–13.
  13. Referans 13 Marmarou CR, Prieto R, Taya K, Young HF, Marmarou A. Marmarou weight drop injury model. Anim Model Acute Neurol Inj. 2009;393–407.
  14. Referans 14 Berikol GB, Berikol G, Ayrik C, Kose A, Babus SB, Gumus LT, et al. Antioxidant and Neuroprotective Effects of L-arginine Administration After Traumatic Brain Injury and Hemorrhagic Shock in Rats. Turk Neurosurg. 2023;33(3):379–85.
  15. Referans 15 Doǧanyiǧit Z, Erbakan K, Akyuz E, Polat AK, Arulsamy A, Shaikh MF. The Role of Neuroinflammatory Mediators in the Pathogenesis of Traumatic Brain Injury: A Narrative Review. ACS Chem Neurosci. 2022;13(13):1835–48.
  16. Referans 16 Webster KM, Sun M, Crack P, O’Brien TJ, Shultz SR, Semple BD. Inflammation in epileptogenesis after traumatic brain injury. J Neuroinflammation. 2017 Jan;14(1):10.
  17. Referans 17 Youn DH, Han SW, Kim JT, Choi H, Lee A, Kim N, et al. Oxiracetam alleviates anti-inflammatory activity and ameliorates cognitive impairment in the early phase of traumatic brain injury. Acta Neurochir (Wien) [Internet]. 2023;165(8):2201–10. Available from: https://doi.org/10.1007/s00701-023-05674-8
  18. Referans 18 Goss JR, Styren SD, Miller PD, Kochanek PM, Palmer AM, Marion DW, et al. Hypothermia attenuates the normal increase in interleukin 1 beta RNA and nerve growth factor following traumatic brain injury in the rat. J Neurotrauma. 1995 Apr;12(2):159–67.
  19. Referans 19 Hutchinson PJ, O’Connell MT, Rothwell NJ, Hopkins SJ, Nortje J, Carpenter KLH, et al. Inflammation in human brain injury: intracerebral concentrations of IL-1alpha, IL-1beta, and their endogenous inhibitor IL-1ra. J Neurotrauma. 2007 Oct;24(10):1545–57.
  20. Referans 20 Rothwell NJ, Strijbos PJ. Cytokines in neurodegeneration and repair. Int J Dev Neurosci Off J Int Soc Dev Neurosci. 1995;13(3–4):179–85.
  21. Referans 21 Rothwell N. Interleukin-1 and neuronal injury: mechanisms, modification, and therapeutic potential. Brain Behav Immun. 2003 Jun;17(3):152–7.
  22. Referans 22 Song H, Ding Z, Chen J, Chen T, Wang T, Huang J. The AMPK-SIRT1-FoxO1-NF-κB signaling pathway participates in hesperetin-mediated neuroprotective effects against traumatic brain injury via the NLRP3 inflammasome. Immunopharmacol Immunotoxicol. 2022 Dec;44(6):970–83.
  23. Referans 23 Casault C, Al Sultan AS, Banoei M, Couillard P, Kramer A, Winston BW. Cytokine Responses in Severe Traumatic Brain Injury: Where There Is Smoke, Is There Fire? Neurocrit Care. 2019 Feb;30(1):22–32.
  24. Referans 24 Zielinski MR, Gibbons AJ. Neuroinflammation, Sleep, and Circadian Rhythms. Front Cell Infect Microbiol. 2022;12(March):1–16.
  25. Referans 25 Posti JP, Takala RSK, Raj R, Luoto TM, Azurmendi L, Lagerstedt L, et al. Admission Levels of Interleukin 10 and Amyloid β 1-40 Improve the Outcome Prediction Performance of the Helsinki Computed Tomography Score in Traumatic Brain Injury. Front Neurol. 2020;11:549527.
  26. Referans 26 El-Menyar A, Asim M, Khan N, Rizoli S, Mahmood I, Al-Ani M, et al. Systemic and cerebro-cardiac biomarkers following traumatic brain injury: an interim analysis of randomized controlled clinical trial of early administration of beta blockers. Sci Rep [Internet]. 2024;14(1):1–17. Available from: https://doi.org/10.1038/s41598-024-70470-y
  27. Referans 27 Gao Y, Zhang H, Wang J, Li F, Li X, Li T, et al. Annexin A5 ameliorates traumatic brain injury-induced neuroinflammation and neuronal ferroptosis by modulating the NF-ĸB/HMGB1 and Nrf2/HO-1 pathways. Int Immunopharmacol. 2023 Jan;114:109619.
  28. Referans 28 Özen I, Clausen F, Flygt J, Marklund N, Paul G. Neutralization of Interleukin 1-beta is associated with preservation of thalamic capillaries after experimental traumatic brain injury. Front Neurol. 2024;15:1378203.
  29. Referans 29 Zhao G, Zhao J, Lang J, Sun G. Nrf2 functions as a pyroptosis-related mediator in traumatic brain injury and is correlated with cytokines and disease severity: a bioinformatics analysis and retrospective clinical study. Front Neurol. 2024;15:1341342.
  30. Referans 30 Chen S-F, Hsu C-W, Huang W-H, Wang J-Y. Post-injury baicalein improves histological and functional outcomes and reduces inflammatory cytokines after experimental traumatic brain injury. Br J Pharmacol. 2008 Dec;155(8):1279–96.