Isoflurane Attenuates Blood–Brain Barrier Disruption in Ipsilateral Hemisphere After Subarachnoid Hemorrhage in Mice

Altay, Orhan; Suzuki, Hitomi; Hasegawa, Yu; Caner, Başak; Krafft, Paul R.; Fujii, Mutsumi; Tang, Jiping; Zhang, Junyi

doi:10.1161/strokeaha.112.661728

Cited by 108 publications

(115 citation statements)

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“…Brain edema is one of the common and important features of both clinical SAH and experimental SAH [29,30]. Brain edema after SAH reflects disruption of the BBB, which is primarily induced by endothelial cells apoptosis, degradation of the basal-lamina by proteases, and diffuse inflammatory reaction [31][32][33].…”

Section: Discussionmentioning

confidence: 99%

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Chen

et al. 2015

Mol Neurobiol

123

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Minocycline has beneficial effects in early brain injury (EBI) following subarachnoid hemorrhage (SAH); however, the molecular mechanisms underlying these effects have not been clearly identified. This study was undertaken to determine the influence of minocycline on inflammation and neural apoptosis and the possible mechanisms of these effects in early brain injury following subarachnoid hemorrhage. SAH was induced by the filament perforation model of SAH in male Sprague-Dawley rats. Minocycline or vehicle was given via an intraperitoneal injection 1 h after SAH induction. Minocycline treatment markedly attenuated brain edema secondary to blood-brain barrier (BBB) dysfunction by inhibiting NLRP3 inflammasome activation, which controls the maturation and release of pro-inflammatory cytokines, especially interleukin-1β (IL-1β). Minocycline treatment also markedly reduced the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL)-positive cells. To further identify the potential mechanisms, we demonstrated that minocycline increased Bcl2 expression and reduced the protein expression of P53, Bax, and cleaved caspase-3. In addition, minocycline reduced the cortical levels of reactive oxygen species (ROS), which are closely related to both NLRP3 inflammasome and P53 expression. Minocycline protects against NLRP3 inflammasome-induced inflammation and P53-associated apoptosis in early brain injury following SAH. Minocycline's anti-inflammatory and anti-apoptotic effect may involve the reduction of ROS. Minocycline treatment may exhibit important clinical potentials in the management of SAH.

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Section: Discussionmentioning

confidence: 99%

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Chen

et al. 2015

Mol Neurobiol

123

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“…Disadvantages of assessing BBB disruption by fluorescent microscopy are that animal subjects must be under anesthesia, which may exert a time-dependent effect on BBB disruption and blood pressure. 30 In addition, visualization is typically limited to superficial vasculature because of poor tissue penetration and light scattering. However, increased penetration can be achieved with the use of near-infrared light.…”

Section: Strokementioning

confidence: 99%

Assessment of Blood–Brain Barrier Disruption in Stroke

Kassner

Merali

2015

Stroke

123

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T he disease burden of acute ischemic stroke (AIS) is rising in the United States and Canada. It is estimated that in the United States 795 000 people have a stroke each year, which amounts to $34 billion in medical expenses and lost productivity.1 Recent trials have shown the potential benefit of procedural thrombectomy in the management of AIS. 2 However, despite substantial research expenditures over the past 2 decades, there have been no new pharmacological agents for the initial treatment of AIS since the approval of recombinant tissue-type plasminogen activator in 1996. Recently, the role of the blood-brain barrier (BBB) in the pathogenesis of AIS has emerged as a focus for new therapeutic strategies. After the onset of AIS, the BBB is rapidly disrupted and this disruption persists for days through the acute and early subacute phases of AIS. The disruption of the BBB can be quantified as an increase in the permeability of the BBB (Figure 1). 4 In the setting of AIS, disruption of the BBB is thought to be a precursor to serious clinical consequences such as hemorrhagic transformation (HT), 5-7 which refers to the development of a hemorrhage within the ischemic brain tissue. Current research is attempting to elucidate the mechanisms of BBB disruption after AIS and develop therapeutic strategies to mitigate the clinical consequences of BBB disruption.Given these developments, a greater number of preclinical and clinical studies are incorporating assessment of BBB disruption into their study designs. Although assessment of BBB disruption may once have been technically difficult, a plethora of methods now exist to assess BBB disruption with relative ease in animal models and humans. When taken together, these methods cover a wide range of temporal and spatial resolutions and permit simultaneous assessment of cell morphology, protein expression and localization, cell electrophysiology, and gross neurological function. An awareness of the specifications and limitations of the methods of assessing BBB disruption is necessary to design effective studies and evaluate the literature.In the present review, we summarize the available methods of assessing BBB permeability in animal models and humans. We strive to highlight the relative strengths and weaknesses of these methods and provide suggestions for study design in stroke research. Finally, we discuss recent translational developments in assessing BBB disruption for the treatment of AIS. Ex Vivo Assessment of BBB DisruptionThe pioneering experiments of Max Lewandowsky first defined the BBB as a dynamic barrier separating the intravascular and extravascular compartments. This laid the groundwork for current methods of assessing BBB disruption in AIS animal models and human trials.8 All methods of assessing BBB disruption are common in their use of tracers, which can be either endogenous if they are naturally found in the blood or exogenous if introduced into the circulation by the experimenter. Table I in the online-only Data Supplement summarizes methods of ass...

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“…Brain samples were weighed, dried in an oven (80˚C) for 72 h and then weighed again. The brain water content (%) was calculated as follows: [(wet weight -dry weight)/wet weight] x 100 (22).…”

Section: Assessment Of Neurological Status By Testing Blood-brain Barmentioning

confidence: 99%

3,4-Dihydroxyphenylethanol alleviates early brain injury by modulating oxidative stress and Akt and nuclear factor-κB pathways in a rat model of subarachnoid hemorrhage

Fu¹,

Hu²

2016

Experimental and Therapeutic Medicine

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Abstract. 3,4-Dihydroxyphenylethanol (DOPET) is a naturally occurring polyphenolic compound, present in olive oil and in the wastewater generated during olive oil processing. DOPET has various biological and pharmacological activities, including anticancer, antibacterial and anti-inflammatory effects. This study was designed to determine whether DOPET alleviates early brain injury (EBI) associated with subarachnoid hemorrhage (SAH) through suppression of oxidative stress and Akt and nuclear factor (NF)-κB pathways. Rats were randomly divided into the following groups: Sham group, SAH group, SAH + vehicle group and SAH + DOPET group. Mortality, blood-brain barrier (BBB) permeability and brain water content were assessed. Oxidative stress, Akt, NF-κB p65 and caspase-3 assays were also performed. DOPET induced a reduction in brain water content, and decreased the BBB permeability of SAH model rats. Furthermore, DOPET effectively controlled oxidative stress, NF-κB p65 and caspase-3 levels, in addition to significantly increasing Akt levels in the cortex following SAH. These results provide evidence that DOPET attenuates apoptosis in a rat SAH model through modulating oxidative stress and Akt and NF-κB signaling pathways.

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Isoflurane Attenuates Blood–Brain Barrier Disruption in Ipsilateral Hemisphere After Subarachnoid Hemorrhage in Mice

Cited by 108 publications

References 10 publications

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Minocycline Protects Against NLRP3 Inflammasome-Induced Inflammation and P53-Associated Apoptosis in Early Brain Injury After Subarachnoid Hemorrhage

Assessment of Blood–Brain Barrier Disruption in Stroke

3,4-Dihydroxyphenylethanol alleviates early brain injury by modulating oxidative stress and Akt and nuclear factor-κB pathways in a rat model of subarachnoid hemorrhage

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