Lipid peroxidation and oedema in experimental brain injury: comparison of treatment with methylprednisolone, tirilazad mesylate and vitamin E

Koç, Rahmi Kemal; Kurtsoy, Ali; Paşaoğlu, Hatîce; Karaküçük, E Inci; Oktem, Ibrahim; Meral, Mehmet

doi:10.1007/s004330050129

Cited by 13 publications

(3 citation statements)

References 41 publications

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“…Alpha tocopherol reduced microscopic brain damage and also promoted nerve regeneration probably by reducing Nogo-A and NgR expression [ 320 ]. Although these behavioral effects are important, a study showed limited efficacy of vitamin E on lipid peroxidation in the acute post-injury phase [ 321 ]; others have demonstrated a later improvement in markers of oxidative stress. Vitamin E could also present neuroprotective effects for TBI associated dementia [ 322 ].…”

Section: Vitamin Supplementationmentioning

confidence: 99%

Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side

Jacquens

Zanier

Degos

et al. 2022

IJMS

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Head trauma is the most common cause of disability in young adults. Known as a silent epidemic, it can cause a mosaic of symptoms, whether neurological (sensory–motor deficits), psychiatric (depressive and anxiety symptoms), or somatic (vertigo, tinnitus, phosphenes). Furthermore, cranial trauma (CT) in children presents several particularities in terms of epidemiology, mechanism, and physiopathology—notably linked to the attack of an immature organ. As in adults, head trauma in children can have lifelong repercussions and can cause social and family isolation, difficulties at school, and, later, socio-professional adversity. Improving management of the pre-hospital and rehabilitation course of these patients reduces secondary morbidity and mortality, but often not without long-term disability. One hypothesized contributor to this process is chronic neuroinflammation, which could accompany primary lesions and facilitate their development into tertiary lesions. Neuroinflammation is a complex process involving different actors such as glial cells (astrocytes, microglia, oligodendrocytes), the permeability of the blood–brain barrier, excitotoxicity, production of oxygen derivatives, cytokine release, tissue damage, and neuronal death. Several studies have investigated the effect of various treatments on the neuroinflammatory response in traumatic brain injury in vitro and in animal and human models. The aim of this review is to examine the various anti-inflammatory therapies that have been implemented.

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Section: Vitamin Supplementationmentioning

confidence: 99%

Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side

Jacquens

Zanier

Degos

et al. 2022

IJMS

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“…Treatment with vitamin E is effective for some forms of cancer, and prevents and repairs cell tissue damage following radiation [169]. In the central nervous system it has been investigated under lesion [176] and TBI models [31,101]. The neuroprotective effects of α-T are primarily mediated by its prevention of free radical propagation via the halting of polyunsaturated fatty acid oxidation chain reactions [20,167].…”

Section: Vitaminsmentioning

confidence: 99%

“…Furthermore, vitamin E reduces amyloidosis and improves cognitive function after repetitive TBI in a model of Alzheimer’s disease [33]. Although these behavioral effects are substantial, one study has shown limited efficacy of vitamin E on lipid peroxidation in the acute post-injury phase [101], but others have highlighted improvements in markers of oxidative stress at later time points [93,167]. Additional studies have demonstrated that extended pretreatment confers the strongest reductions in lipid peroxidation and oxidative stress [55,209].…”

Section: Vitaminsmentioning

confidence: 99%

Vitamins and nutrients as primary treatments in experimental brain injury: Clinical implications for nutraceutical therapies

et al. 2016

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With the numerous failures of pharmaceuticals to treat traumatic brain injury in humans, more researchers have become interested in combination therapies. This is largely due to the multimodal nature of damage from injury, which causes excitotoxicity, oxidative stress, edema, neuroinflammation and cell death. Polydrug treatments have the potential to target multiple aspects of the secondary injury cascade, while many previous therapies focused on one particular aspect. Of specific note are vitamins, minerals and nutrients that can be utilized to supplement other therapies. Many of these have low toxicity, are already FDA approved and have minimal interactions with other drugs, making them attractive targets for therapeutics. Over the past 20 years, interest in supplementation and supraphysiologic dosing of nutrients for brain injury has increased and indeed many vitamins and nutrients now have a considerable body of literature backing their use. Here, we review several of the prominent therapies in the category of nutraceutical treatment for brain injury in experimental models, including vitamins (B2, B3, B6, B9, C, D, E), herbs and traditional medicines (ginseng, gingko biloba), flavonoids, and other nutrients (magnesium, zinc, carnitine, omega-3 fatty acids). While there is still much work to be done, several of these have strong potential for clinical therapies, particularly with regard to polydrug regimens.

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The lazaroid tirilazad is a new inhibitor of direct and indirect UVA-induced lipid peroxidation in human dermal fibroblasts

Dissemond

Schneider

Wlaschek

et al. 2003

Archives of Dermatological Research

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Lipid peroxidation caused by oxidative stress within the tissue leads to destruction and dysfunction of cellular membranes. Human dermal fibroblasts in the skin are subject to constant photooxidative stress caused mainly by deeply penetrating UVA irradiation. Therefore, the membrane damage caused by this photooxidative stress may be a major promoter of photoaging and photocarcinogenic processes initiated and promoted by long-term UVA exposure of the skin. The oxidative destruction is counterbalanced by a complex network of enzymatic and nonenzymatic antioxidants creating the skin's line of defence against UVA-induced reactive oxygen species. The lazaroid tirilazad represents a new synthetic group of antioxidants with structural molecular similarity to glucocorticosteroids. We investigated the antioxidative capacity of tirilazad by determining its effects on the levels of malondialdehyde (MDA), as a marker of lipid peroxidation, induced directly or indirectly by UVA in human dermal fibroblasts. In a time- and dose-dependent kinetic, we demonstrated that fibroblasts incubated with tirilazad are well protected against subsequent UVA irradiation and show no increase in MDA levels similar to the unirradiated controls. This was also observed when lipid peroxidation was caused chemically by incubation of human dermal fibroblasts with 200 micro M Fe(3+)-citrate and 1 m M ascorbyl phosphate as a model of indirect UVA-induced skin damage. Lysates of fibroblasts treated this way showed a tenfold increase in MDA levels, whereas preincubation with tirilazad resulted in a significantly lower increase in MDA levels. Furthermore, in a comparison with the well-established radical scavenger Trolox, an alpha-tocopherol analogue, tirilazad offered better protection to the membranes. Our results demonstrate for the first time that the lazaroid tirilazad is an effective inhibitor of direct and indirect UVA-induced increases in MDA as a marker of lipid peroxidation in human dermal fibroblasts.

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Lipid peroxidation and oedema in experimental brain injury: comparison of treatment with methylprednisolone, tirilazad mesylate and vitamin E

Cited by 13 publications

References 41 publications

Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side

Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side

Vitamins and nutrients as primary treatments in experimental brain injury: Clinical implications for nutraceutical therapies

The lazaroid tirilazad is a new inhibitor of direct and indirect UVA-induced lipid peroxidation in human dermal fibroblasts

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