Changes in the cerebrospinal fluid lipid profile following subarachnoid hemorrhage in a closed cranium model: Correlations to cerebral vasospasm, neuronal cell death and Interleukin-6 synthesis. A pilot study

2020 ◽  
Vol 29 (9) ◽  
pp. 105054
Author(s):  
Davide Croci ◽  
Edin Nevzati ◽  
Carl Muroi ◽  
Salome Schöpf ◽  
Thorsten Hornemann ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebrospinal Fluid ◽  
Subarachnoid Hemorrhage ◽  
Pilot Study ◽  
Lipid Profile ◽  
Cerebral Vasospasm ◽  
Interleukin 6 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Neuroprotection after Hemorrhagic Stroke Depends on Cerebral Heme Oxygenase-1

Antioxidants ◽  
2019 ◽  
Vol 8 (10) ◽  
pp. 496 ◽  
Author(s):  
Sandra Kaiser ◽  
Sibylle Frase ◽  
Lisa Selzner ◽  
Judith-Lisa Lieberum ◽  
Jakob Wollborn ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebrospinal Fluid ◽  
Functional Outcome ◽  
Signaling Pathway ◽  
Heme Oxygenase ◽  
Hemorrhagic Stroke ◽  
Mrna Level ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Heme Oxygenase 1

(1) Background: A detailed understanding of the pathophysiology of hemorrhagic stroke is still missing. We hypothesized that expression of heme oxygenase-1 (HO-1) in microglia functions as a protective signaling pathway. (2) Methods: Hippocampal HT22 neuronal cells were exposed to heme-containing blood components and cell death was determined. We evaluated HO-1-induction and cytokine release by wildtype compared to tissue-specific HO-1-deficient (LyzM-Cre.Hmox1 fl/fl) primary microglia (PMG). In a study involving 46 patients with subarachnoid hemorrhage (SAH), relative HO-1 mRNA level in the cerebrospinal fluid were correlated with hematoma size and functional outcome. (3) Results: Neuronal cell death was induced by exposure to whole blood and hemoglobin. HO-1 was induced in microglia following blood exposure. Neuronal cells were protected from cell death by microglia cell medium conditioned with blood. This was associated with a HO-1-dependent increase in monocyte chemotactic protein-1 (MCP-1) production. HO-1 mRNA level in the cerebrospinal fluid of SAH-patients correlated positively with hematoma size. High HO-1 mRNA level in relation to hematoma size were associated with improved functional outcome at hospital discharge. (4) Conclusions: Microglial HO-1 induction with endogenous CO production functions as a crucial signaling pathway in blood-induced inflammation, determining microglial MCP-1 production and the extent of neuronal cell death. These results give further insight into the pathophysiology of neuronal damage after SAH and the function of HO-1 in humans.

Tocilizumab Reduces Vasospasms, Neuronal Cell Death, and Microclot Formation in a Rabbit Model of Subarachnoid Hemorrhage

2021 ◽  
Author(s):  
Davide M. Croci ◽  
Stefan Wanderer ◽  
Fabio Strange ◽  
Basil E. Grüter ◽  
Sivani Sivanrupan ◽  
...  
Keyword(s):  
Cell Death ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Cell Death ◽  
Rabbit Model ◽  
Neuronal Cell

scholarly journals Hemoglobin and Iron Handling in Brain after Subarachnoid Hemorrhage and the Effect of Deferoxamine on Early Brain Injury

2010 ◽  
Vol 30 (11) ◽  
pp. 1793-1803 ◽  
Author(s):  
Jin-Yul Lee ◽  
Richard F Keep ◽  
Yangdong He ◽  
Oren Sagher ◽  
Ya Hua ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Subarachnoid Hemorrhage ◽  
Neuronal Cell Death ◽  
Iron Concentration ◽  
Neuronal Cell ◽  
Nonheme Iron ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Tunel Staining ◽  
Heme Oxygenase 1

The purpose of this study was to investigate hemoglobin and iron handling after subarachnoid hemorrhage (SAH), examine the relationship between iron and neuroglial cell changes, and determine whether deferoxamine (DFX) can reduce SAH-induced injury. The SAH was induced in Sprague-Dawley rats ( n=110) using an endovascular perforation technique. Animals were treated with DFX (100 mg/kg) or vehicle 2 and 6 hours after SAH induction followed by every 12 hours for 3 days. Rats were killed at 6 hours, Days 1 and 3 to determine nonheme iron and examine iron-handling proteins using Western blot and immunohistochemistry. 8-Hydroxyl-2′-deoxyguanosine and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining were performed to assess oxidative DNA damage and neuronal cell death. After SAH, marked heme-oxygenase-1 (HO-1) upregulation at Day 3 ( P<0.01) was accompanied by elevated nonheme iron ( P<0.01), transferrin (Tf) ( P<0.01), Tf receptor ( P<0.05), and ferritin levels ( P<0.01). Deferoxamine treatment reduced SAH-induced mortality (12% versus 29%, P<0.05), brain nonheme iron concentration, iron-handling protein expression, oxidative stress, and neuronal cell death at Day 3 ( P<0.01) after SAH. These results suggest that iron overload in the acute phase of SAH causes oxidative injury leading to neuronal cell death. Deferoxamine effectively reduced oxidative stress and neuronal cell death, and may be a potential therapeutic agent for SAH.

Argon treatment alters microglial activation and neuronal cell death after experimental subarachnoid hemorrhage – a randomized controlled animal trial

2019 ◽  
Author(s):  
Benedikt Kremer ◽  
Mark Coburn ◽  
Agnieszka Weinandy ◽  
Kay Nolte ◽  
Hans Clusmann ◽  
...  
Keyword(s):  
Cell Death ◽  
Subarachnoid Hemorrhage ◽  
Microglial Activation ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Control Group ◽  
Cortical Region ◽  
Significant Difference ◽  
Experimental Subarachnoid Hemorrhage

Abstract Background Here, we demonstrate argon´s neuroprotective and immunomodulatory properties after experimental subarachnoid hemorrhage (SAH) examining various localizations (hippocampal and cortical regions) with respect to neuronal damage and microglial activation 6, 24 and 72h after SAH. Methods One hour after SAH (endovascular perforation rat model) or sham surgery, a gas mixture containing 50 vol% argon (argon group) or 50 vol% nitrogen (control group) was applied for 1h. Cerebral coronal sections (H&E; Iba-1 stained) were analyzed for neuronal cell death and microglial activation in predefined anatomical regions. Results Comparing the hippocampal regions 6h after SAH reduced neuronal damage was seen in the argon group (p<0.0001) as well as in the cortical region (p=0.014). Over time the effect diminished: A substantial difference 24h after SAH was only seen for the cortical region (p=0.004). No significant difference was observed 72h after SAH. The hippocampal and overall microglial activation 24h after SAH were significantly reduced in the argon group (p=0.013; p<0.0001), whereas 72h after SAH significance was only detected in the cortical area (p=0.014). Conclusion Argon treatment ameliorated early neuronal damage after SAH. However, inhibition of microglial activation might indicate a beneficial effect with regard to secondary inflammatory.

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