SavedAdd your journal

Journals / SDÜ Tıp Fakültesi Dergisi / 2024 / Cilt: 31 Sayı: 4

Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage

Ali Serdar Oğuzoğlu(Süleyman Demirel Üniversitesi Tıp Fakültesi)0000-0002-1735-4062
Halil Aşçı(SÜLEYMAN DEMİREL ÜNİVERSİTESİ)0000-0002-1545-035X
Musa Canan(SÜLEYMAN DEMİREL ÜNİVERSİTESİ)0009-0005-7279-0026
Nilgün Şenol(SÜLEYMAN DEMİREL ÜNİVERSİTESİ)0000-0002-1714-3150
Özlem Özmen(BURDUR MEHMET AKİF ERSOY ÜNİVERSİTESİ)0000-0002-1835-1082
Pages
310–317
Publication Date
2024-12-26
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage (SAH) can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis.
📊
Key Findings & Data:This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH.
💡
Conclusion & Impact:Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.
🔬Design:Araştırma Makalesi
📍Scope:Comprehensive Sample
⚙️Variables:Subarachnoid hemorrhage · Liver · Lung

Abstract

Objective: Oxidant and inflammatory substances released into the blood due to subarachnoidal hemorrhage (SAH) can pass into the peripheral compartment, causing distant organ damage due to blood-brain barrier permeability caused by oxidative stress, inflammation, and apoptosis. This study aimed to demonstrate the secondary damage to peripheral organs, including the lung, kidney, and liver, resulting from SAH. Material and Method: Twenty rats were divided into sham and SAH groups, each consisting of ten animals. In the SAH group animals, 0.3 mL autologous blood taken from the tail artery was injected into the cisterna magna for 2 minutes. Seven days after SAH formation, all animals were euthanized under anesthesia. Following decapitation, brain tissues, lung, liver, and kidney tissues were placed in 10% formaldehyde for histopathological and immunohistochemical analysis. Results: In the SAH group, neuronal degeneration in the cerebral cortex, and hyperemia and hemorrhage in the lung, kidney, and liver were observed histopathologically. In immunohistochemical examinations, decreased expression of brain-derived neurotrophic factor (BDNF) and neurofilament (NF) in the cerebral cortex, cerebellum, and hippocampus sections; In lung tissues, enhanced caspase (Cas)-3, hypoxia-inducible factor 1 alpha (Hif-1α) and nuclear factor kappa beta (NF-κB) expressions in the lung, Cas-5, cyclooxygenase-1 (Cox-1) and interleukin (IL)-1 expressions in the liver, Cas-3, Cox-1 and IL-3 expressions in the kidney were observed. Conclusion: Following SAH, in addition to damage to brain tissue, peripheral tissues such as the lung, kidney, and liver can also be damaged through inflammation and apoptosis.

🔖

Cite This Article

Oğuzoğlu, A. S., Aşçı, H., Canan, M., Şenol, N., Özmen, Ö. (2024). Inflammation and Apoptosis-Related Damage in Lung, Liver, and Kidney Tissues due to Subarachnoidal Hemorrhage. SDÜ Tıp Fakültesi Dergisi, Cilt: 31 Sayı: 4, 310–317. https://doi.org/10.17343/sdutfd.1482851

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (24)

  1. Van Gijn J, Kerr RS, Rinkel GJ. Subarachnoid hemorrhage. The Lancet 2007;369(9558):306-18.
  2. Tujjar O, Belloni I, Hougardy J-M, Scolletta S, Vincent J-L, Creteur J, Taccone FS. Acute kidney injury after subarachnoid hemorrhage. Journal of Neurosurgical Anesthesiology 2017;29(2):140-9.
  3. Mukandala G, Tynan R, Lanigan S, O’Connor JJ. The effects of hypoxia and inflammation on synaptic signaling in the CNS. Brain Sciences 2016;6(1):6.
  4. Nguyen A, Patel AB, Kioutchoukova IP, Diaz MJ, Lucke-Wold B. Mechanisms of mitochondrial oxidative stress in Brain Injury: from pathophysiology to therapeutics. Oxygen 2023;3(2):163-78.
  5. Zhao Y, Gan L, Ren L, Lin Y, Ma C, Lin X. Factors influencing the blood-brain barrier permeability. Brain Research 2022;1788:147937.
  6. Wang Z, Zhou F, Dou Y, Tian X, Liu C, Li H, et al. Melatonin alleviates intracerebral hemorrhage-induced secondary brain injury in rats via suppressing apoptosis, inflammation, oxidative stress, DNA damage, and mitochondria injury. Translational Stroke Research 2018;9:74-91.
  7. Senol N, Oguzoglu AS, Erzurumlu Y, Ascı H, Savran M, Gulle K, et al. Modulation of salubrinal-mediated endoplasmic reticulum stress in an experimental subarachnoid hemorrhage model. World Neurosurgery 2021;153:e488-e96.
  8. Chen S, Li Q, Wu H, Krafft PR, Wang Z, Zhang JH. The harmful effects of subarachnoid hemorrhage on extracerebral organs. BioMed Research is International 2014;2014(1):858496.
  9. Bernardo-Castro S, Sousa JA, Brás A, Cecília C, Rodrigues B, Almendra L, et al. Pathophysiology of blood-brain barrier permeability throughout the different stages of ischemic stroke and its implication on hemorrhagic transformation and recovery. Frontiers in Neurology 2020;11:594672.
  10. Jiang X, Andjelkovic AV, Zhu L, Yang T, Bennett MV, Chen J, et al. Blood-brain barrier dysfunction and recovery after ischemic stroke. Progress in Neurobiology 2018;163:144-71.
  11. Han DW, Oh JE, Lim BJ, Han Y, Song Y. Dexmedetomidine attenuates subarachnoid hemorrhage-induced acute lung injury through regulating autophagy and TLR/NFκB signaling pathway. Korean J Anesthesiol 2022;75:518-29.
  12. Li T, Wang P, Gong X, Chong W, Hai Y, You C, et al. Prevalence and prognostic significance of liver fibrosis in patients with aneurysmal subarachnoid hemorrhage. Frontiers in Neurology 2022;13:850405.
  13. Mobed A, Charsouei S, Yazdani Y, Gargari MK, Ahmadalipour A, Sadremousavi SR, et al. Biosensors, recent advances in the determination of BDNF and NfL. Cellular and Molecular Neurobiology 2023;43(8):3801-14.
  14. Zhou J, Guo P, Guo Z, Sun X, Chen Y, Feng H. Fluid metabolic pathways after subarachnoid hemorrhage. Journal of Neurochemistry 2022;160(1):13-33.
  15. Alfonso M, Aftab S, Hamadneh T, Sherali N, Tsouklidis N. Understanding cognitive deficit after subarachnoid hemorrhage: a memory focused approach. Cureus 2020;12(11).
  16. Chen H, Dang Y, Liu X, Ren J, Wang H. Exogenous brain‑derived neurotrophic factor attenuates neuronal apoptosis and neurological deficits after subarachnoid hemorrhage in rats. Experimental and Therapeutic Medicine 2019;18(5):3837-44.
  17. Demedts IK, Demoor T, Bracke KR, Joos GF, Brusselle GG. Role of apoptosis in the pathogenesis of COPD and pulmonary emphysema. Respiratory Research 2006;7:1-10.
  18. Suresh MV, Yalamanchili G, Rao TC, Aktay S, Kralovich A, Shah YM, Raghavendran K. Hypoxia‐inducible factor (HIF)‐1α‐induced regulation of lung injury in pulmonary aspiration is mediated through NF‐kB. FASEB BioAdvances 2022;4(5):309.
  19. Sargon MF. Lungs and hypoxia: a review of the literature. Anatomy 2021;15(1):76-83.
  20. Pereira M, Liang J, Edwards-Hicks J, Meadows AM, Hinz C, Liggi S, et al. Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting. Cell Reports 2024;43(2).
  21. Galea J, Ogungbenro K, Hulme S, Patel H, Scarth S, Hoadley M, et al. Reduction of inflammation after administration of interleukin-1 receptor antagonist following aneurysmal subarachnoid hemorrhage: results of the Subcutaneous Interleukin-1Ra in SAH (SCIL-SAH) study. Journal of Neurosurgery 2017;128(2):515-23.
  22. Hvas C, Nørregaard R, Nielsen T, Barklin A, Tønnesen E. Brain death increases COX‐1 and COX‐2 expression in the renal medulla in a pig model. Acta Anaesthesiologica Scandinavica 2014;58(2):243-50.
  23. Priante G, Gianesello L, Ceol M, Del Prete D, Anglani F. Cell death in the kidney. International Journal of Molecular Sciences 2019;20(14):3598.
  24. Ratliff BB, Abdulmahdi W, Pawar R, Wolin MS. Oxidant mechanisms in renal injury and disease. Antioxidants & Redox Signaling 2016;25(3):119-46.