The antioxidative, non-psychoactive tricyclic phenothiazine reduces brain damage after experimental traumatic brain injury in mice

Songarj, Phuriphong; Luh, Clara; Staib-Lasarzik, Irina; Engelhard, Kristin; Moosmann, Bernd; Thal, Serge C.

doi:10.1016/j.neulet.2014.10.037

Cited by 20 publications

(10 citation statements)

References 33 publications

(51 reference statements)

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“…Bearing in mind the neuroprotective effects of structurally related drugs in adult brain injury models ( Geng et al, 2017 ; Songarj et al, 2015 ), the next step was to assess LMP in an animal model of neonatal excitotoxic brain injury. Owing to its long biological half-life ( Dahl, 1976 ), a single i.p.…”

Section: Discussionmentioning

confidence: 99%

The effect of levomepromazine on the healthy and injured developing mouse brain – An in vitro and in vivo study

et al. 2020

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Section: Discussionmentioning

confidence: 99%

The effect of levomepromazine on the healthy and injured developing mouse brain – An in vitro and in vivo study

et al. 2020

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“…These preparations were hematoxylin/eosin (HE) or Iba-1 stained and examined with light microscope at 20x zoom for differences in the number of neurons or microglia cells. Therefore, parts of cornu ammonis (CA1 and CA2) were chosen as regions of interest and a 1950 x 1936 pixel large picture was examined [ 12 ].…”

Section: Methodsmentioning

confidence: 99%

Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model

et al. 2018

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IntroductionThe acute respiratory distress syndrome is not only associated with a high mortality, but also goes along with cognitive impairment in survivors. The cause for this cognitive impairment is still not clear. One possible mechanism could be cerebral inflammation as result of a “lung-brain-crosstalk”. Even mechanical ventilation itself can induce cerebral inflammation. We hypothesized, that an acute lung injury aggravates the cerebral inflammation induced by mechanical ventilation itself and leads to neuronal damage.MethodsAfter approval of the institutional and state animal care committee 20 pigs were randomized to one of three groups: lung injury by central venous injection of oleic acid (n = 8), lung injury by bronchoalveolar lavage in combination with one hour of injurious ventilation (n = 8) or control (n = 6). Brain tissue of four native animals from a different study served as native group. For six hours all animals were ventilated with a tidal volume of 7 ml kg-1 and a scheme for positive end-expiratory pressure and inspired oxygen fraction, which was adapted from the ARDS network tables. Afterwards the animals were killed and the brains were harvested for histological (number of neurons and microglia) and molecular biologic (TNFalpha, IL-1beta, and IL-6) examinations.ResultsThere was no difference in the number of neurons or microglia cells between the groups. TNFalpha was significantly higher in all groups compared to native (p < 0.05), IL-6 was only increased in the lavage group compared to native (p < 0.05), IL-1beta showed no difference between the groups.DiscussionWith our data we can confirm earlier results, that mechanical ventilation itself seems to trigger cerebral inflammation. This is not aggravated by acute lung injury, at least not within the first 6 hours after onset. Nevertheless, it seems too early to dismiss the idea of lung-injury induced cerebral inflammation, as 6 hours might be just not enough time to see any profound effect.

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“…The CCI model was initially characterized and refined using pneumatic devices [ 12 , 13 , 14 ]. Today, pneumatic CCI devices remain popular [ 18 , 19 , 20 , 21 , 22 ], with several commercially available models. Notably, electromagnetic devices have become commercially available and have been adopted by many research teams [ 23 , 24 , 25 , 26 ].…”

Section: Model Overviewmentioning

confidence: 99%

Mini Review of Controlled Cortical Impact: A Well-Suited Device for Concussion Research

Osier

Dixon

2017

Brain Sciences

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Mild traumatic brain injury (mTBI) is increasingly recognized as a significant public health problem which warrants additional research. Part of the effort to understand mTBI and concussion includes modeling in animals. Controlled cortical impact (CCI) is a commonly employed and well-characterized model of experimental TBI that has been utilized for three decades. Today, several commercially available pneumatic- and electromagnetic-CCI devices exist as do a variety of standard and custom injury induction tips. One of CCI’s strengths is that it can be scaled to a number of common laboratory animals. Similarly, the CCI model can be used to produce graded TBI ranging from mild to severe. At the mild end of the injury spectrum, CCI has been applied in many ways, including to study open and closed head mTBI, repeated injuries, and the long-term deficits associated with mTBI and concussion. The purpose of this mini-review is to introduce the CCI model, discuss ways the model can be applied to study mTBI and concussion, and compare CCI to alternative pre-clinical TBI models.

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The antioxidative, non-psychoactive tricyclic phenothiazine reduces brain damage after experimental traumatic brain injury in mice

Cited by 20 publications

References 33 publications

The effect of levomepromazine on the healthy and injured developing mouse brain – An in vitro and in vivo study

The effect of levomepromazine on the healthy and injured developing mouse brain – An in vitro and in vivo study

Lung injury does not aggravate mechanical ventilation-induced early cerebral inflammation or apoptosis in an animal model

Mini Review of Controlled Cortical Impact: A Well-Suited Device for Concussion Research

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