Decreased neutrophil levels in mice with traumatic brain injury after cape administration

et al. 2020

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Introduction Head injury is an injury or wound of the brain tissue due to external forces; it can cause a decrease or change in the status of consciousness. Many head injury models have used mice as experimental animals; the Marmarou model is the most famous and the most widely-used diffuse brain injury model. In this study, we slightly modified the Marmarou model. The purpose of this study is to help researchers examining head injuries in mice, especially those in developing countries who have limited facilities and infrastructure. Methods This experimental research uses animals models ( Rattus novergicus , strain Sprague Dawley) that fit several criteria, including male, aged 10–12 weeks, and body weight of 200–300 g. This study involves a slight modification on the tube used, with a 20 cm-long weight of 20 g. The blood samples for the following assays of ELISA and brain tissue samples were collected at 24 h and 4, 5, 6, and 7 days post-trauma. Results A significant effect on the brain was seen with the Marmarou model modification, at a mass weight of 20 g and height of 20 cm, with 0.04 J energy produced. Changes were also seen in the histological features of brain tissue and the serum levels of AQP-4, F2 IsoPs, MPO, and VEGF from 24 h until 7 days after trauma. Conclusion This report describes the development of an experimental head injury approach modifying the Marmarou model that is able to produce a diffuse brain injury model in mice.

Section: Discussionmentioning

confidence: 99%

Modification of the Marmarou model in developing countries

Nasution

et al. 2020

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“…This pro-inflammatory mediators will upregulate chemotaxis and chemoattractant leading to leukocyte activation as an immune response as shown by neutrophils accumulation in the brain after a brain injury. There has been shown from previous study that metalloproteinase protein (MPO) is increased in brain injury, but its correlation with HMGB1 level in yet not known [ 7 , 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

“…Inflammation after TBI is now has been recognized as complex interaction between central and peripheral cellular and soluble components. Previous study revealed that CAPE can reduce Neutrophil serum levels there by preventing brain damage in TBI [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Immunomodulatory properties of high mobility group box 1 and its potential role in brain injury: Review article

Tommy

et al. 2020

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Background Human mobility group box 1 (HMGB1) is a novel biomolecular agent which has a major part in inflammation process. HMGB1 has been known to be a strong pro-inflammatory factor as damage associated molecular pattern (DAMP) which its interaction with its receptor, the receptor of advanced glycation end products (RAGE), will cause positive amplification of inflammation signalling pathway. Brain injury is one of the major contributors for disability and death which neuroinflammation has a major role in its pathogenesis and influencing its outcome. In neuroinflammation, it has been described that HMGB1 may have a pivotal role in the process. Objective The objective of this article is to review the role HMGB1 in brain injury and its immunomodulatory properties. Methods A comprehensive search of literature was conducted in PubMed (NIH), Scopus, EMBASE, and Google Scholar database using keyword combinations of the medical subject headings (MeSH) of “HMGB1” and “Brain Injury” and relevant reference lists were also manually searched. All relevant articles of any study design published from year 1990 till June 2020, were included and narratively discussed in this review. Results Twenty-four articles were shortlisted and reviewed in this article. Through these articles, we synthesis information on the function and metabolism of HMGB1, immunomodulatory effect of HMGB1, clinical findings and other potential treatment involving HMGB1, and role of HMGB1 protein in brain injury. Conclusion HMGB1 has a strong pro-inflammation property which predominantly acts through RAGE pathways.Review registration number reviewregistry966 in www.researchregistry.com .

“…Rats were induced with ketamine which had been diluted at a dose of 3-10 mg/kg, a head injury in accordance with the modified Marmarou model was conducted [ 21 , 22 ]. The surgical procedure began with the aseptic procedure using povidone iodine, then a coronal incision was made through the center of the skull and then a burr holes was performed using a high-speed drill until the duramater was exposed; a 1.5 cm long craniectomy was done, then a mass of 20 g was dropped from a height of 20 cm by passing through a tube posing as a transport medium, the area with the exposed duramater was placed just below the opening of the tube, so that the mass [ 23 ] lands exactly on the area of the head which had the duramater exposed, to ensure the trauma model has caused damage to the brain, 1 rat was put down for pathology examination with hematoxylin staining, the results were hemorrhage in the brain tissue, while other rats were treated according to post-craniotomy procedure protocols, lastly all wounds were sutured using zyde 5.0 after antibiotic ointment was administered.…”

Section: Methodsmentioning

confidence: 99%

Role of CAPE in reducing oxidative stress in animal models with traumatic brain injury

Nasution

et al. 2020

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Introduction The central nervous system (CNS) is the most metabolically active organ characterized by high oxygen demand and relatively low anti-oxidative activity, which makes neurons and glia highly susceptible to damage by reactive oxygen and nitrogen byproducts as well as neurodegeneration. Free radicals are associated with secondary injuries that occur after a primary brain injury. Some of these free radical products include F2-Isoprostane (F2-IsoPs), malondialdehyde (MDA), 4-hydroxy-2-nonenal (4-HNE) and acrolein. Methods In this study we measured serum F2-IsoPs levels as markers of free radical activity in 10–12 week-old male Sprague-Dawley rats weighing 200–300 g, all rats (n = 10) subjected with a head injury according to the modified marmourou model, then divided into 2 groups, one group treated with CAPE (Caffeic Acid Phenethyl Ester) (n = 5) and the other not treated with CAPE (n = 5), serum levels in the two groups were compared starting from day-0 (before brain injury), day-4 and day-7. Results We found lower F2-IsoPs levels in the group that received the CAPE treatment compared to the group that did not receive the CAPE treatment. Conclusion CAPE is capable of significantly reducing oxidative stress in brain injury.