Traumatic brain injury: clinical and pathological parameters in an experimental weightdrop model

Silva, Danilo dos Santos; Brito, José Nazareno Pearce de Oliveira; Ibiapina, Jerúsia Oliveira; Lima, Marcel Fernando Miranda Batista; Medeiros, Andréa Ribeiro Gonçalves de Vasconcelos; Queiroz, BÃ¡rbara Hamedy Carvalho E.; Guedes, Vanessa Olímpio de Melo

doi:10.1590/s0102-86502011000200004

Cited by 9 publications

(5 citation statements)

References 16 publications

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“…For the weight-drop model, this model is limited in the production of primary lesions that are macroscopically meaningful once it is not capable of creating cranial fractures with levels of energy compatible with life after impact. It presented discrete focal lesions in a small number of animals and only at elevated levels of energy, but in accordance with what was described in similar studies [ 59 ]. Moreover, any single animal model may not be able to fully mimic the highly heterogeneous nature of human TBI [ 60 ].…”

Section: Discussionsupporting

confidence: 91%

Evidence-based review of oral traditional Chinese medicine compound recipe administration for treating weight drop-induced experimental traumatic brain injury

Yang

Wang

Sheng

et al. 2016

BMC Complement Altern Med

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BackgroundRecently, a number of studies conducted and published in China have suggested that traditional Chinese medicine compound recipe (TCMCR) may be beneficial in the treatment of experimental traumatic brain injury (TBI). In this study, we conducted a systematic review and meta-analysis of the efficacy of TCMCR in TBI model with weight drop method to provide robust evidence on the effects of TCMCR and to determine whether TCMCR can be recommended for routine treatment or considered as a standard treatment for TBI.MethodsWe identified eligible studies by searching five electronic databases on April 1, 2014, and pooled the data using the random-effects model. Results were reported in terms of standardized mean difference (SMD). We also calculated statistical heterogeneity, evaluated the studies’ methodological quality and investigated the presence of publication bias.ResultsTotally, 187 relevant publications were searched from databases, 25 of which met our inclusion criteria. The overall methodological quality of the most studies was poor, and there was evidence of statistical heterogeneity among studies along with small-study effects. Meta-analysis showed statistically significant effects indicating that TCMCR has a beneficial effect on TBI.ConclusionsDespite the limitations, we concluded that TCMCR may reduce brain water content, improve BBB permeability, and decrease TNF-α/NO expression after experimental TBI in terms of overall efficacy. However, our review also indicates that more well-designed and well-reported animal studies are needed.

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Section: Discussionsupporting

confidence: 91%

Evidence-based review of oral traditional Chinese medicine compound recipe administration for treating weight drop-induced experimental traumatic brain injury

Yang

Wang

Sheng

et al. 2016

BMC Complement Altern Med

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“…The force to be applied to the head was determined not to exceed 0.5 joules so that the animals would survive the head injury and maintain their nourishment functions. For this purpose, we used weight and height upper limits of 50 g and 1 m, respectively [9].…”

Section: Methodsmentioning

confidence: 99%

Investigation of the effects of inflammatory and metabolic factors on fracture union in head trauma and long bone fractures

et al. 2023

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Background/Aim: Fractures are the most common form of trauma in current orthopedic practice. Although studies have shed light on the relationship between the factors affecting the healing process after fracture, this process is still not fully understood. In this study, we aimed to investigate the changes in serum biomediator levels and fracture healing in different trauma patterns, such as head trauma (HT), long bone fracture (LBF), a combination of HT + LBF injury (CI), and in different time points of the healing period. Methods: Forty Wistar rats were included in the study and divided into five groups. Group 1, the donor group, included rats with HT; Group 2 included rats with LBFs who were administered the serum taken from rats in Group 1; Group 3 included the rats with isolated LBFs; and Group 4 the rats with CI. Group 5 comprised the control rats. An experimental closed HT and fracture model was applied to rats. The rats in Groups 2, 3 and 4 were sacrificed on the 10th, 20th, and 30th days. The biomediator levels in the serum taken after sacrification were studied, while closed femoral fracture models were examined radiologically. Results: Statistically significant differences were found among the groups regarding radiological scores on the 10th, 20th, and 30th days. On Day 10, Group 2a had significantly higher scores than Group 3a (P=0.03), and Group 3a had lower scores than Group 4a (P=0.01). On Day 20, Group 2b had significantly higher scores than Group 3b (P=0.004) but lower than Group 4b (P=0.03). On Day 30, Group 2c had significantly higher scores than Group 3c but lower than Group 4c (P=0.001). The mean Ca, TGF beta 1, beta-catenin, IL-10, IL-17A, TNF alpha, CRP, Wnt-16, ALP, GH, PTH, IL-1 beta, IL-6, and IL-22 levels were significantly different among the groups (P<0.05). No significant difference was observed in the biomediator levels among the groups at different time points of the healing period. Conclusion: We concluded that inflammatory cytokines (IL-1 beta, IL-6, IL-17A, IL-17F, IL-23, and TNF alpha) were elevated in the early period in individuals with isolated head trauma and that this effect could be transferred to other individuals by serum transfer. On the other hand, the negative relationship between the IL-10 level, which is a negative modulator in fracture union, and callus thickness was significant. Our study contributes by providing a molecular description of the positive union effect transferred between individuals by serum. We believe our findings will play a significant role in developing new therapeutic agents for fracture healing.

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“…In order to mimic human diffuse TBI caused by falls or motor vehicle accidents, we used the Marmarou’s impact acceleration model (Marmarou´s IAM) that recreates global impact on the brain ( Foda and Marmarou, 1994 ; Marmarou et al, 1994 ; Silva et al, 2011 ; Xiong et al, 2013 ). For this purpose, animals were anesthetized (Ketamine 55 mg/kg/xylazine 11 mg/kg) and subjected to a controlled TBI, described elsewhere ( Marmarou et al, 1994 ; Silva et al, 2011 ). Briefly, the “trauma device” consists of 1 m removable aluminum tube, attached to a wooden platform, which allows a controlled impact when dropping a 45 gr brass sphere onto a stainless steel disc located above the animal head, causing a 0.45J impact when it is dropped from the mentioned height.…”

Section: Methodsmentioning

confidence: 99%

Early IGF-1 Gene Therapy Prevented Oxidative Stress and Cognitive Deficits Induced by Traumatic Brain Injury

et al. 2021

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Traumatic Brain Injury (TBI) remains a leading cause of morbidity and mortality in adults under 40 years old. Once primary injury occurs after TBI, neuroinflammation and oxidative stress (OS) are triggered, contributing to the development of many TBI-induced neurological deficits, and reducing the probability of critical trauma patients´ survival. Regardless the research investment on the development of anti-inflammatory and neuroprotective treatments, most pre-clinical studies have failed to report significant effects, probably because of the limited blood brain barrier permeability of no-steroidal or steroidal anti-inflammatory drugs. Lately, neurotrophic factors, such as the insulin-like growth factor 1 (IGF-1), are considered attractive therapeutic alternatives for diverse neurological pathologies, as they are neuromodulators linked to neuroprotection and anti-inflammatory effects. Considering this background, the aim of the present investigation is to test early IGF-1 gene therapy in both OS markers and cognitive deficits induced by TBI. Male Wistar rats were injected via Cisterna Magna with recombinant adenoviral vectors containing the IGF-1 gene cDNA 15 min post-TBI. Animals were sacrificed after 60 min, 24 h or 7 days to study the advanced oxidation protein products (AOPP) and malondialdehyde (MDA) levels, to recognize the protein oxidation damage and lipid peroxidation respectively, in the TBI neighboring brain areas. Cognitive deficits were assessed by evaluating working memory 7 days after TBI. The results reported significant increases of AOPP and MDA levels at 60 min, 24 h, and 7 days after TBI in the prefrontal cortex, motor cortex and hippocampus. In addition, at day 7, TBI also reduced working memory performance. Interestingly, AOPP, and MDA levels in the studied brain areas were significantly reduced after IGF-1 gene therapy that in turn prevented cognitive deficits, restoring TBI-animals working memory performance to similar values regarding control. In conclusion, early IGF-1 gene therapy could be considered a novel therapeutic approach to targeting neuroinflammation as well as to preventing some behavioral deficits related to TBI.

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Traumatic brain injury: clinical and pathological parameters in an experimental weightdrop model

Abstract: The experimental cranium trauma animal model by weight drop is an alternative of low cost and easy reproduction that allows evaluating clinical and pathological alterations in accordance with studies in experimental surgery aims for new traumatic brain injury approach in rats.

Cited by 9 publications

References 16 publications

Evidence-based review of oral traditional Chinese medicine compound recipe administration for treating weight drop-induced experimental traumatic brain injury

Evidence-based review of oral traditional Chinese medicine compound recipe administration for treating weight drop-induced experimental traumatic brain injury

Investigation of the effects of inflammatory and metabolic factors on fracture union in head trauma and long bone fractures

Early IGF-1 Gene Therapy Prevented Oxidative Stress and Cognitive Deficits Induced by Traumatic Brain Injury

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