Reducing the incidence and mortality of traumatic brain injury in Latin America.

Traumatic brain injury (TBI) represents a considerable portion of the global injury burden. The incidence of TBI will continue to increase in view of an increase in population density, an aging population, and the increased use of motor vehicles, motorcycles, and bicycles. The most common causes of TBI are falls and road traffic injuries. Deaths related to road traffic injury are three times higher in low-and middle-income countries (LMIC) than in high-income countries (HIC). The Latin American Caribbean region has the highest incidence of TBI worldwide, primarily caused by road traffic injuries. Data from HIC indicates that road traffic injuries can be successfully prevented through concerted efforts at the national level, with coordinated and multisector responses to the problem. Such actions require implementation of proven measures to address the safety of road users and the vehicles themselves, road infrastructure, and post-crash care. In this review, we focus on the epidemiology of TBI in Latin America and the implementation of solutions and preventive measures to decrease mortality and long-term disability.

Full-face motorcycle helmets to reduce injury and death: A systematic review, meta-analysis, and practice management guideline from the Eastern Association for the Surgery of Trauma.

BACKGROUND: While motorcycle helmets reduce mortality and morbidity, no guidelines specify which is safest. We sought to determine if full-face helmets reduce injury and death. METHODS: We searched for studies without exclusion based on: age, language, date, or randomization. Case reports, professional riders, and studies without original data were excluded. Pooled results were reported as OR (95% CI). Risk of bias and certainty was assessed. (PROSPERO #CRD42021226929). RESULTS: Of 4431 studies identified, 3074 were duplicates, leaving 1357 that were screened. Eighty-one full texts were assessed for eligibility, with 37 studies (n = 37,233) eventually included. Full-face helmets reduced traumatic brain injury (OR 0.40 [0.23-0.70]); injury severity for the head and neck (Abbreviated Injury Scale [AIS] mean difference -0.64 [-1.10 to -0.18]) and face (AIS mean difference -0.49 [-0.71 to -0.27]); and facial fracture (OR 0.26 [0.15-0.46]). CONCLUSION: Full-face motorcycle helmets are conditionally recommended to reduce traumatic brain injury, facial fractures, and injury severity.

Reducing the Neurotrauma Burden in India-A National Mobilization.

India has one of the highest TBI burdens due to road traffic accidents (RTAs), with 60% of head injuries being attributable to RTA and more than 150,000 lives being lost annually due to traumatic brain injury (TBI). These numbers have prompted institutions and organizations at international, national, and local levels to mobilize and address this burden through prevention, prehospital care, and in hospital care. Academic institutions such as Andhra Medical College have run local campaigns promoting the wearing of helmets when riding 2-wheelers. Prehospital care institutions such as Gunupati Venkata Krishna - Emergency Management and Research Institute have also made large strides nationally on delivering safe and timely care through novel and focused education to its emergency medical technicians, applying evidence-based practice to all facets of its work. These changes led to implementation of novel and innovative technological solutions for faster and more efficient responses. National institutions such as the Neurological Society of India (NSI) and Neurotrauma Society of India (NTSI) have been instrumental in promoting safety measures such as use of helmets and seatbelts through social media videos, often using celebrities to disseminate the message. NSI have also focused on sharing best practices for the management of TBI through easy-to-use platforms such as YouTube. Institutions such as American Association of Physicians of Indian Origin, NSI, and NTSI have collaboratively developed TBI management guidelines that are specific to the Indian population (supported by American Association of South Asian Neurosurgeons). Non-governmental organizations such as the Indian Head Injury Foundation and Save Life Foundation have contributed to this movement by promoting awareness through campaigns and public education. While TBI remains a large burden in India, a mobilization and coalesced efforts of such a scale holds promise for tackling this burden.

Analyzing pediatric bicycle injuries using geo-demographic data.

PURPOSE: Bicycle accidents are potentially preventable, and helmets can mitigate the severity of injuries. The purpose of the study it to investigate geo-demographic areas to establish prevention policies and targeted programs. METHODS: From October 2013 to March 2020 all bicycle injuries at a Level 1 trauma center were collected for ages ≤18 years. Demographics, injuries, and outcomes were analyzed. Incidents were aggregated to zip codes and the Local Indicators of Spatial Association (LISA) statistic was used to test for spatial clustering of injury rates per 10,000 children. RESULTS: Over the 8-year time period, 77 cases were identified with an average age of 13±4 years, 83% male and 48% non-Hispanic white. The majority of patients (98%) were not wearing a helmet. Loss of consciousness was reported in 44% and 21% sustained a traumatic brain injury. Twenty-eight percent required ICU care and 36% required operative interventions. There was only 1 mortality in the cohort (<1%).Injuries were more common in lower household income zip codes (Figure 1). Six zip codes encompassing several interstate exits and the connected heavy-traffic roadways comprise a statistically significant cluster of pediatric bicycle accidents (Figure 1). CONCLUSION: Low-income neighborhoods and those near major roadways held the highest risk for pediatric bicycle accidents. Use of helmets was extremely low in the patient population, with high rates of traumatic brain injury. With this information, targeted programs to address high-risk intersections, helmet access, and safety education can be implemented locally.

Comparing the medical coverage provided by four contemporary military combat helmets against penetrating traumatic brain injury.

INTRODUCTION: Modern military combat helmets vary in their shapes and features, but all are designed to protect the head from traumatic brain injury. Recent recommendations for protection against energised projectiles that are characteristic of secondary blast injury is to ensure coverage of both the brain and brainstem. METHOD: Graphical representations of essential coverage of the head (cerebral hemispheres, cerebellum and brainstem) within an anthropometrically sized model were superimposed over two standard coverage helmets (VIRTUS helmet, Advanced Combat Helmet (ACH)) and two 'high-cut' helmets (a Dismounted Combat Helmet (DCH)) and Combat Vehicle Crewman (CVC) helmet), both of which are designed to be worn with communications devices. Objective shotline coverage from representative directions of projectile travel (-30 to +30 degrees) was determined using the Coverage of Armour Tool (COAT). RESULTS: VIRTUS and ACH demonstrated similar overall coverage (68.7% and 69.5%, respectively), reflecting their similar shell shapes. ACH has improved coverage from below compared with VIRTUS (23.3% vs 21.7%) due to its decreased standoff from the scalp. The 'high-cut' helmets (DCH and CVC) had reduced overall coverage (57.9% and 52.1%), which was most pronounced from the side. CONCLUSIONS: Both the VIRTUS and ACH helmets provide excellent overall coverage of the brain and brainstem against ballistic threats. Coverage of both would be improved at the rear by using a nape protector and the front using a visor. This is demonstrated with the analysis of the addition of the nape protector in the VIRTUS system. High-cut helmets provide significantly reduced coverage from the side of the head, as the communication devices they are worn with are not designed to provide protection from ballistic threats. Unless absolutely necessary, it is therefore recommended that high-cut helmets be worn only by those users with defined specific requirements, or where the risk of injury from secondary blast is low.

Brain Protection after Anoxic Brain Injury: Is Lactate Supplementation Helpful?

While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.

Activation peptide of coagulation factor IX improves the prognosis after traumatic brain injury.

Recently, coagulation factor IX and its activation peptide have been reported to suppress the permeability of vascular endothelial cells. In this study, the therapeutic effects of a synthesized activation peptide is investigated in traumatic brain injury model rats. In cerebral contusion, dysfunction of the blood brain barrier with increasing vascular permeability promotes the progression of neuropathy after injury. The model rats were generated by controlled cortical impact. Then, rats were intravenously injected with 350 µg/kg of the synthesized activation peptide or PBS as a control, every day for a month. Behavioral studies were conducted during a month of observation. For morphological analysis, macro- and microscopic observation were performed. Water content of brain tissue was used to assess edema. To assess the function of blood brain barrier, Evans Blue method was employed. In the neurological examinations and beam-walking, the treated rats performed significantly better than control rats. Measurements of cerebral defect volume showed that the treatment significantly reduced it by 82%. Nissl stain showed that neural cells adjacent to impacts were lost in control rats, but saved in treated rats. The treatment significantly reduced brain edema and extravascular leakage of Evans blue. Intravenous injection with a synthesized activation peptide significantly reduced damage to neural tissue and improved neural functioning in the model rats.

Acute treatment with TrkB agonist LM22A-4 confers neuroprotection and preserves myelin integrity in a mouse model of pediatric traumatic brain injury.

Young children have a high risk of sustaining a traumatic brain injury (TBI), which can have debilitating life-long consequences. Importantly, the young brain shows particular vulnerability to injury, likely attributed to ongoing maturation of the myelinating nervous system at the time of insult. Here, we examined the effect of acute treatment with the partial tropomyosin receptor kinase B (TrkB) agonist, LM22A-4, on pathological and neurobehavioral outcomes after pediatric TBI, with the hypothesis that targeting TrkB would minimize tissue damage and support functional recovery. We focused on myelinated tracts-the corpus callosum and external capsules-based on recent evidence that TrkB activation potentiates oligodendrocyte remyelination. Male mice at postnatal day 21 received an experimental TBI or sham surgery. Acutely post-injury, extensive cell death, a robust glial response and disruption of compact myelin were evident in the injured brain. TBI or sham mice then received intranasal saline vehicle or LM22A-4 for 14 days. Behavior testing was performed from 4 weeks post-injury, and brains were collected at 5 weeks for histology. TBI mice showed hyperactivity, reduced anxiety-like behavior, and social memory impairments. LM22A-4 ameliorated the abnormal anxiolytic phenotype but had no effect on social memory deficits. Use of spectral confocal reflectance microscopy detected persistent myelin fragmentation in the external capsule of TBI mice at 5 weeks post-injury, which was accompanied by regionally distinct deficits in oligodendrocyte progenitor cells and post-mitotic oligodendrocytes, as well as chronic reactive gliosis and atrophy of the corpus callosum and injured external capsule. LM22A-4 treatment ameliorated myelin deficits in the perilesional external capsule, as well as tissue volume loss and the extent of reactive gliosis. However, there was no effect of this TrkB agonist on oligodendroglial populations detected at 5 weeks post-injury. Collectively, our results demonstrate that targeting TrkB immediately after TBI during early life confers neuroprotection and preserves myelin integrity, and this was associated with some improved neurobehavioral outcomes as the pediatric injured brain matures.

Mer regulates microglial/macrophage M1/M2 polarization and alleviates neuroinflammation following traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) is a leading cause of death and disability worldwide. Microglial/macrophage activation and neuroinflammation are key cellular events following TBI, but the regulatory and functional mechanisms are still not well understood. Myeloid-epithelial-reproductive tyrosine kinase (Mer), a member of the Tyro-Axl-Mer (TAM) family of receptor tyrosine kinases, regulates multiple features of microglial/macrophage physiology. However, its function in regulating the innate immune response and microglial/macrophage M1/M2 polarization in TBI has not been addressed. The present study aimed to evaluate the role of Mer in regulating microglial/macrophage M1/M2 polarization and neuroinflammation following TBI. METHODS: The controlled cortical impact (CCI) mouse model was employed. Mer siRNA was intracerebroventricularly administered, and recombinant protein S (PS) was intravenously applied for intervention. The neurobehavioral assessments, RT-PCR, Western blot, magnetic-activated cell sorting, immunohistochemistry and confocal microscopy analysis, Nissl and Fluoro-Jade B staining, brain water content measurement, and contusion volume assessment were performed. RESULTS: Mer is upregulated and regulates microglial/macrophage M1/M2 polarization and neuroinflammation in the acute stage of TBI. Mechanistically, Mer activates the signal transducer and activator of transcription 1 (STAT1)/suppressor of cytokine signaling 1/3 (SOCS1/3) pathway. Inhibition of Mer markedly decreases microglial/macrophage M2-like polarization while increases M1-like polarization, which exacerbates the secondary brain damage and sensorimotor deficits after TBI. Recombinant PS exerts beneficial effects in TBI mice through Mer activation. CONCLUSIONS: Mer is an important regulator of microglial/macrophage M1/M2 polarization and neuroinflammation, and may be considered as a potential target for therapeutic intervention in TBI.

Preventive effects of seat belts on traumatic brain injury in motor vehicle collisions classified by crash severities and collision directions.

PURPOSE: This study aimed to measure the preventive effect of seat belt on traumatic brain injury (TBI) and to compare the effect according to the crash severities and collision directions. METHODS: Korea In-Depth Accident Study (KIDAS) has collected vehicle and demographic data on injured occupants involved in motor vehicle collisions (MVCs) who visited three emergency medical centers for calendar years 2011-2016. Primary and secondary end points were TBI (abbreviated injury score 2+) and in-hospital mortality. Crush extent (CE) was classified into 1-2, 3-4, 5-6, and 7-9 according to the crash severity. We calculated adjusted odds ratios (ORs) of seat belts and CE for study outcomes and developed an interaction model in each collision direction using multivariate logistic regression analysis. RESULTS: Of the 2,245 occupants who were injured in MVCs, 295 (13.1%) occupants sustained TBI. In univariate analysis, old age, unbelted status, lateral collision, and higher CE were factors associated with TBI in MVCs. Occupants with belted status was less likely to have TBI and in-hospital mortality compared with those with unbelted status [AORs (95% CI) 0.48 (0.37-0.62) and 0.49 (0.30-0.81), respectively]. In interaction analysis, preventive effects of seat belts on TBI from MVCs were retained within CE 5-6 in frontal MVCs and within CE 1-2 in near side lateral MVCs, and those of seat belts on in-hospital mortality were reserved within CE 3-4 in frontal and rollover MVCs. CONCLUSIONS: The preventive effects of seat belts on TBI and in-hospital mortality are preserved within a limited crash severity in each collision direction.

Modulation of Brain Transcriptome by Combined Histone Deacetylase Inhibition and Plasma Treatment Following Traumatic Brain Injury and Hemorrhagic Shock.

INTRODUCTION: We previously showed that the addition of valproic acid (VPA), a histone deacetylase inhibitor, to fresh frozen plasma (FFP) resuscitation attenuates brain lesion size and swelling following traumatic brain injury (TBI) and hemorrhagic shock (HS). The goal of this study was to use computational biology tools to investigate the effects of FFP+VPA on the brain transcriptome following TBI+HS. METHODS: Swine underwent TBI+HS, kept in shock for 2 h, and resuscitated with FFP or FFP + VPA (n = 5/group). After 6 h of observation, brain RNA was isolated and gene expression was analyzed using a microarray. iPathwayGuide, Gene Ontology (GO), Gene-Set Enrichment Analysis, and Enrichment Mapping were used to identify significantly impacted genes and transcriptomic networks. RESULTS: Eight hundred differentially expressed (DE) genes were identified out of a total of 9,118 genes. Upregulated genes were involved in promotion of cell division, proliferation, and survival, while downregulated genes were involved in autophagy, cell motility, neurodegenerative diseases, tumor suppression, and cell cycle arrest. Seven hundred ninety-one GO terms were significantly enriched. A few major transcription factors, such as TP53, NFKB3, and NEUROD1, were responsible for modulating hundreds of other DE genes. Network analysis revealed attenuation of interconnected genes involved in inflammation and tumor suppression, and an upregulation of those involved in cell proliferation and differentiation. CONCLUSION: Overall, these results suggest that VPA treatment creates an environment that favors production of new neurons, removal of damaged cells, and attenuation of inflammation, which could explain its previously observed neuroprotective effects.

Modeling of post-traumatic epilepsy and experimental research aimed at its prevention

Research on the prevention of post-traumatic epilepsy (PTE) has seen remarkable advances regarding its physiopathology in recent years. From the search for biomarkers that might be used to indicate individual susceptibility to the development of new animal models and the investigation of new drugs, a great deal of knowledge has been amassed. Various groups have concentrated efforts in generating new animal models of traumatic brain injury (TBI) in an attempt to provide the means to further produce knowledge on the subject. Here we forward the hypothesis that restricting the search of biomarkers and of new drugs to prevent PTE by using only a limited set of TBI models might hamper the understanding of this relevant and yet not preventable medical condition.

Impact of helmet laws on motorcycle crash mortality rates.

BACKGROUND: Helmets are effective in reducing traumatic brain injury. However, population effects of helmet laws have not been well described. This study assesses the impact of helmet laws on the motorcycle (MC) fatality rate in the United States from 1999 to 2015. METHODS: Fatality Analysis Reporting System MC fatalities (aged ≥16 years), crash characteristics, and MC-related laws were collected by year for all 50 states from 1999 to 2015 to create a pooled time series. Generalized linear autoregressive modeling was applied to assess the relative contribution of helmet laws to the MC fatality rate while controlling for other major driver laws and crash characteristics. RESULTS: Universal helmet laws were associated with a 36% to 45% decline in the motorcycle crash mortality rate during the study period across all age cohorts (unstandardized regression coefficients are reported): 16 to 20 years, B = -0.45 (p < 0.05); 21 to 55 years, B = -0.42 (p < 0.001); 56 to 65 years, B = -0.38 (p < 0.04); and older than 65 years, B = -0.36 (p < 0.02). Partial helmet laws were associated with a 1% to 81% increase in the fatality rate compared with states with no helmet laws and a 22% to 45% increase compared with universal laws. Helmet usage did not attenuate the countervailing effect of weaker partial laws for 16 to 20 years (B = 0.01 [p < 0.001]). Other laws associated with a declining motorcycle crash mortality rate included the following: social host/overservice laws, 21 to 55 years (B = -0.38 [p < 0.001]); 56 to 65 years (B = -0.16 [p < 0.002]), and older than 65 years (B = -0.12 [p < 0.003]); laws reducing allowable blood alcohol content, 21 to 55 years (B = -4.9 [p < 0.02]); and laws limiting passengers for new drivers 16 to 20 years (B = -0.06 [p < 0.01]). CONCLUSION: During the period of the study, universal helmet laws were associated with a declining mortality rate, while partial helmet laws were associated with an increasing mortality rate. Other state driver laws were also associated with a declining rate. In addition to universal helmet laws, advocating for strict alcohol control legislation and reevaluation of licenses in older riders could also result in significant reduction in MC-related mortality. LEVEL OF EVIDENCE: Prognostic and epidemiological, level III.

Docosahexaenoic Acid Protects Traumatic Brain Injury by Regulating NOX2 Generation via Nrf2 Signaling Pathway.

Docosahexaenoic acid (DHA) is verified to have neuroprotective effects on traumatic brain injury (TBI) rats by activating Nrf2 signaling pathway, but the role of NOX2 in this effect has not been illuminated. So this study explored the role of NOX2 in TBI models treated with DHA, aiming to complete the mechanism of DHA. TBI rat models were constructed with or without DHA treatment, and H2O2-induced hippocampal neurons were pretreated with DHA alone or in combination with Nrf2 inhibitor brusatol. The neurological function, cognitive ability, and cerebral edema degree of rats were assessed. The apoptosis rate and viability of cells was measured. The generation of NOX2, Nrf2, HO-1 and NQO-1 expression levels, and ROS content in hippocampal CA1 region and hippocampal neurons were detected. DHA could not only improve the neurological function, brain edema and cognitive ability in TBI rats, but also decrease effectively the contents of NOX2 and ROS in hippocampal CA1 region and hippocampal neurons. DHA promoted the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal CA1 region and hippocampal neurons. On the contrary, Nrf2 inhibitor brusatol inhibited the nuclear transposition of Nrf2 and the expression levels of HO-1 and NQO-1 in hippocampal neurons, promoted the generation of ROS and NOX2, and accelerated cell apoptosis. Both in vivo and in vitro experiments demonstrated that DHA treated TBI by reducing NOX2 generation that might function on Nrf2 signaling pathway, providing a potential evidence for its clinical application.

Estrogen Formation and Inactivation Following TBI: What we Know and Where we Could go.

Traumatic brain injury (TBI) is responsible for various neuronal and cognitive deficits as well as psychosocial dysfunction. Characterized by damage inducing neuroinflammation, this response can cause an acute secondary injury that leads to widespread neurodegeneration and loss of neurological function. Estrogens decrease injury induced neuroinflammation and increase cell survival and neuroprotection and thus are a potential target for use following TBI. While much is known about the role of estrogens as a neuroprotective agent following TBI, less is known regarding their formation and inactivation following damage to the brain. Specifically, very little is known surrounding the majority of enzymes responsible for the production of estrogens. These estrogen metabolizing enzymes (EME) include aromatase, steroid sulfatase (STS), estrogen sulfotransferase (EST/SULT1E1), and some forms of 17ß-hydroxysteroid dehydrogenase (HSD17B) and are involved in both the initial conversion and interconversion of estrogens from precursors. This article will review and offer new prospective and ideas on the expression of EMEs following TBI.

TGFß1 alleviates axonal injury by regulating microglia/macrophages alternative activation in traumatic brain injury.

Traumatic brain injury (TBI) causes substantial mortality and long-term disability worldwide. TGFß1 is a unique molecular and functional signature in microglia, but the role of TGFß1 in TBI is not clear. The purpose of this study was to investigate the role of TGFß1 in TBI. The weight dropping device was used to establish TBI model of rats. Hematoxylin eosin staining and Bielschowsky silver staining were used to assess tissue loss. Beam walking and muscle strength tests were used to assess neurological deficits. Immunohistochemical staining was used to assess axonal injures. Western blotting was used to detect expression of related proteins. RT-PCR was used to detect expression of cytokines. Immunofluorescence staining was used to assess the microglia/macrophages activation. We observed obvious axonal injury and microglia/macrophages activation in the peri-lesion cortex. The expression of inflammatory cytokines was markedly high after TBI. The expression of TGFß1 and TGFßRI were significantly reduced after TBI. TGFß1 promoted the functional recovery and alleviated axonal injury 1 day after TBI. TGFß1 promoted microglia/macrophages polarizing to alternative activation and alleviated neuroinflammation. These effects of TGFß1 could be inhibited by LY2109761, the inhibitor of TGFRI/II. These results suggested that TGFß1 played a protective role in axonal injury and could be a potential therapeutic target in early stages following TBI.

An Effective NADPH Oxidase 2 Inhibitor Provides Neuroprotection and Improves Functional Outcomes in Animal Model of Traumatic Brain Injury.

Traumatic brain injury (TBI) has become a leading cause of death and disability all over the world. Pharmacological suppression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) can inhibit oxidative stress which is implicated in the pathology of TBI. GSK2795039 was reported to target NOX2 to inhibit [Formula: see text] and ROS production. The present study aimed to investigate the effect of GSK2795039 on NOX2 activity and neurological deficits in a TBI mouse model. TBI mouse model was established by a weight-drop to mouse skull. GSK2795039 at a dose of 100 mg/kg was administrated to mice 30 min before TBI. NOX2 expression and activity were detected by Western blot and biochemical method. Neurological damage and apoptosis were detected by behavioral test and terminal deoxynucleotidyl transferase dUTP nick end labeling staining. GSK2795039 significantly inhibited NOX2 expression and activity in the TBI mouse model. It also attenuated TBI-induced neurological deficits, apoptosis, and neurological recovery. The results indicate that GSK2795039 can be used as a potential drug for TBI treatment.

The effect of rosmarinic acid on deformities occurring in brain tissue by craniectomy method. Histopathological evaluation of IBA-1 and GFAP expressions

Abstract Purpose To investigate the role of Rosmarinic acid (RA) in the prevention of traumatic brain injury and the immunohistochemical analysis of IBA-1 and GFAP expressions. Methods Healthy male rats were randomly divided into 3 groups consisting of 10 rats. Groups were as follows; control group, traumatic brain injury (TBI) group, and TBI+RA group. After traumatic brain injury, blood samples were taken from the animals and analyzed with various biochemical markers. And then IBA-1 and GFAP expressions were evaluated immunohistochemically. Results Significant results were obtained in all biochemical parameters between groups. Immunohistochemical sections showed IBA-1 not only in microglia and macrophage activity but also in degenerative neurons in blood vessel endothelial cells. However, GFAP reaction and post-traumatic rosmarinic acid administration showed positive expression in astrocytes with regular structure around the blood vessel. Conclusion Rosmarinic acid in blood vessel endothelial cells showed that preserving the integrity of astrocytic structure in the blood brain barrier may be an important antioxidant.

Medicinal plants in traumatic brain injury: Neuroprotective mechanisms revisited.

Traumatic brain injury (TBI) is the most prevalent health problem affecting all age groups, and leads to many secondary problems in other organs especially kidneys, gastrointestinal tract, and heart function. In this review, the search terms were TBI, fluid percussion injury, cold injury, weight drop impact acceleration injury, lateral fluid percussion, cortical impact injury, and blast injury. Studies with Actaea racemosa, Artemisia annua, Aframomum melegueta, Carthamus tinctorius, Cinnamomum zeylanicum, Crocus sativus, Cnidium monnieri, Curcuma longa, Gastrodia elata, Malva sylvestris, Da Chuanxiong Formula, Erigeron breviscapus, Panax ginseng, Salvia tomentosa, Satureja khuzistanica, Nigella sativa, Drynaria fortune, Dracaena cochinchinensis, Polygonum cuspidatum, Rosmarinus officinalis, Rheum tanguticum, Centella asiatica, and Curcuma zedoaria show a significant decrease in neuronal injury by different mechanisms such as increasing superoxide dismutase and catalase activities, suppressing nuclear factor kappa B (NF-κB), interleukin 1 (IL-1), glial fibrillary acidic protein, and IL-6 expression. The aim of this study was to evaluate the neuroprotective effects of medicinal plants in central nervous system pathologies by reviewing the available literature.