scholarly journals X-linked inhibitor of apoptosis inhibits apoptosis and preserves the blood-brain barrier after experimental subarachnoid hemorrhage

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Cheng Gao ◽  
Hongwei Yu ◽  
Cong Yan ◽  
Wenyang Zhao ◽  
Yao Liu ◽  
...  
Neurosurgery ◽  
1992 ◽  
Vol 30 (6) ◽  
pp. 882-886 ◽  
Author(s):  
Antonino Germanó ◽  
Domenico dʼAvella ◽  
Rocco Cicciarello ◽  
Ronald L. Hayes ◽  
Francesco Tomasello

1983 ◽  
Vol 58 (3) ◽  
pp. 338-344 ◽  
Author(s):  
Eric W. Peterson ◽  
Erico R. Cardoso

✓ In three groups of cats, the authors studied the effect of subarachnoid hemorrhage (SAH) on the permeability of the blood-brain barrier (BBB) to the penetration of Evans blue-protein complex. One group received arterial hypertension alone, one group SAH alone, and one group SAH followed by arterial hypertension. Animals subjected to arterial hypertension alone showed areas of BBB breakdown. However, when cats were rendered hypertensive after SAH, there were no demonstrable BBB lesions. The SAH was produced by intracisternal injection of whole blood and hypertension by the intravenous injection of metaraminol. The preservation of the BBB after SAH is discussed. Vasospasm is considered as a possible hemodynamic variable responsible for the protection of the BBB from hypertensive damage. The need for a new model is proposed to further investigate the state of the BBB after SAH.


2022 ◽  
Vol 2022 ◽  
pp. 1-13
Author(s):  
Yongfa Zhang ◽  
Baocheng Gao ◽  
Jingsong Ouyang ◽  
Bai Tai ◽  
Shuai Zhou

Subarachnoid hemorrhage (SAH) is a kind of severe hemorrhagic stroke, and early brain injury acted as one of the main causes of death and delayed neurological deficit in patients with subarachnoid hemorrhage. In this process, the function and structural integrity of the blood-brain barrier play an important role. In this study, we have observed whether the apolipoprotein E (apoE) mimetic peptide, COG133, can alleviate early brain injury after subarachnoid hemorrhage. For this purpose, an experimental subarachnoid hemorrhage model was constructed in mice and treated by intravenous injection of COG133 at a dosage of 1 mg/kg. Then, the function and integrity of the blood-brain barrier were detected, and the pyroptosis level of the neuron was determined. The results showed that COG133 could protect blood-brain barrier function and structure integrity, reduce early brain injury, and ameliorate neurological function after subarachnoid hemorrhage. In terms of molecular mechanism, COG133 inhibits blood-brain barrier destruction through the proinflammatory CypA-NF-κB-MMP9 pathway and reduces neuronal pyroptosis by inhibiting NLRP3 inflammasome activation. In conclusion, this study demonstrated that apoE-mimetic peptide, COG133, can play a neuroprotective role by protecting blood-brain barrier function and inhibiting brain cell pyroptosis to reduce early brain injury after subarachnoid hemorrhage.


2018 ◽  
Vol 10 (5) ◽  
pp. 534-545 ◽  
Author(s):  
Clara Luh ◽  
Sergej Feiler ◽  
Katrin Frauenknecht ◽  
Simon Meyer ◽  
Lubomir T. Lubomirov ◽  
...  

Neurosurgery ◽  
1992 ◽  
Vol 30 (6) ◽  
pp. 882-886
Author(s):  
Antonino Germanó ◽  
Domenico d'Avella ◽  
Rocco Cicciarello ◽  
Ronald L. Hayes ◽  
Francesco Tomasello

1986 ◽  
Vol 6 (6) ◽  
pp. 650-657 ◽  
Author(s):  
N. Aa. Svendgaard ◽  
T. J. Delgado ◽  
A. Brun

Intracisternal injection of blood in the rat induced an angiographically demonstrable biphasic cerebral vasospasm with a maximal acute spasm at 10 min and a maximal late spasm at 2 days after the subarachnoid hemorrhage. Systemic administration of 6-hydroxydopamine, which destroys catecholamine fibers in the circumventricular areas characterized by the absence of a blood–brain barrier, prevented the development of both the acute and the late spasm. Isolation or removal of one of the circumventricular organs, the pituitary, from the brain via a stalk transection or a hypophysectomy did not affect the degree of vasospasm. Lesion of the median eminence, another region without a blood–brain barrier, prevented the development of both types of spasm. The median eminence receives projections from the A1 and A2 nuclei in the medulla oblongata. It is suggested that the projections of these nuclei to the internal layer of the median eminence underlie the development of spasm.


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