Cytokines and Perinatal Brain Damage

Dammann, Olaf; O’Shea, T. Michael

doi:10.1016/j.clp.2008.07.011

Cited by 177 publications

(150 citation statements)

References 192 publications

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“…This is supported by epidemiological evidence linking materno-fetal infection and inflammation with brain injury and neonatal encephalopathy at birth [2,3] and elevated proinflammatory cytokines in fetal blood and amniotic fluid in neonates with brain damage [4,5,6]. Moreover, endotoxin infusion in animal models is associated with increased circulating proinflammatory cytokine concentrations and white matter injury [7,8,9].…”

Section: Introductionmentioning

confidence: 51%

Inhibition of Matrix Metalloproteinases-2/-9 Transiently Reduces Pre-Oligodendrocyte Loss during Lipopolysaccharide- but Not Tumour Necrosis Factor-alpha-Induced Inflammation in Fetal Ovine Glial Culture

Weaver-Mikaere¹,

Gunn

Mitchell³

et al. 2013

Dev Neurosci

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To determine whether increased matrix metalloproteinase (MMP) proteolytic activity plays a pathological role in infection/inflammation-induced preterm brain injury, primary cultures of preterm (day 90 of gestation; term 145 days) fetal ovine mixed glia were exposed to 24-96 h of lipopolysaccharide (LPS, 1 μg/ml) or tumour necrosis factor-α (TNF-α, 100 ng/ml). MMP-2 mRNA levels were significantly increased after TNF-α (96 h) and LPS exposure (48 and 96 h), and MMP-9 mRNA levels were significantly increased at 48 and 96 h after TNF-α. On zymography, the active form of secreted MMP-2 was significantly increased 24 h after LPS, but not TNF-α. Both active and latent forms of MMP-9 gelatinolytic activity were significantly increased by TNF-α (96 h) and LPS (72 and 96 h). On reverse zymography, inhibitory activity of TIMP-1 but not TIMP-2 was significantly increased by TNF-α and LPS. SB-3CT-mediated MMP-2 and MMP-9 inhibition transiently reduced LPS-induced oligodendrocyte cell death but had no effect during TNF-α exposure. Collectively, these observations suggest a limited, transient effect of MMPs on immature white matter damage associated with infection but not TNF-α-mediated inflammation.

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Section: Introductionmentioning

confidence: 51%

Inhibition of Matrix Metalloproteinases-2/-9 Transiently Reduces Pre-Oligodendrocyte Loss during Lipopolysaccharide- but Not Tumour Necrosis Factor-alpha-Induced Inflammation in Fetal Ovine Glial Culture

Weaver-Mikaere¹,

Gunn

Mitchell³

et al. 2013

Dev Neurosci

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“…12 Cerebral palsy is also caused by damage pertained to the brain and its cells. 13 Hence a disease caused due to injury to vital organs; here brain, can cause a disease of vata which helps us understand cerebral palsy in the light of vata vyadhi; diseases caused due to vitiated vata. There are eighty diseases of vata and the clinical presentations of cerebral palsy can be appreciated among them.…”

Section: Discussionmentioning

confidence: 99%

A Review on Cerebral Palsy in Children: Bridging Ayurvedic Concepts With Scientific Approaches in Medicine

Raj¹,

Viswaroopan²,

Shailaja³

et al. 2017

Int. J. Res. Ayurveda Pharm.

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Cerebral Palsy is a neurological disorder caused by a non-progressive brain injury or malformation that occurs while a child's brain is under development. It is the most common cause for motor disability in children. Population-based studies from around the world report prevalence estimates of Cerebral Palsy ranging from 1.5 to more than 4 per 1,000 live births or children of a defined age range. 2.3 to 3.6 out of every 1,000 children is the rate of occurrence of Cerebral Palsy. Spastic Cerebral Palsy constitutes about 61 percent to 76.9 percent of all Cerebral Palsy cases. There is no single disease or condition explained in classical texts of Ayurveda regarding Cerebral Palsy. But various conditions have been discussed which can be critiqued and understood as different presentations of cerebral palsy. The present paper details the available Ayurveda descriptions of Cerebral Palsy in line with the modern scientific considerations on the same.

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“…Следующим важным фактором ГИП является воспаление. Целый ряд исследований отслежи-вает связь ГИП с повышенным уровнем воспалительных цитокинов [58][59][60], а также с активацией генов воспа-ления [61]. Наиболее важную роль воспаление играет во второй фазе ГИП (от 6 до 48 ч).…”

Section: обзор литературыunclassified

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

Каркашадзе¹,

Аникин²,

Зимина³

et al. 2016

Pediatr. farmakol.

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ВВЕДЕНИЕ Общемировой научно-технический прогресс в отно-шении исследовательских технологий за последние де-сятилетия привел к качественному и количественно-му скачку нейронаук. Наиболее активно наполняется новыми данными поле фундаментальных представлений о развитии головного мозга, что обусловливает интересы ученых к таким областям медицины, как перинатальная неврология и неврология раннего возраста. Несмотря на расширение представлений о вкладе генетической составляющей, по-прежнему большое внимание уделяет-ся изучению прямых патофизиологических механизмов гипоксически-ишемических поражений (ГИП) головного мозга у новорожденных. К настоящему моменту накоплен массив новых данных в этой области, что подталкивает медицину к внедрению передовых лечебных технологий.Цель работы -провести литературный обзор совре-менных научных данных о механизмах гипоксически-ише-мических повреждений мозга у новорожденных и разра-батываемых на их основании новых методов лечения. ПАТОФИЗИОЛОГИЧЕСКИЕ МЕХАНИЗМЫ ГИПОКСИЧЕСКИ-ИШЕМИЧЕСКИХ ПОРАЖЕНИЙТрадиционно основные лечебные тактики в острый период гипоксически-ишемических перинатальных поражений головного мозга (ГИППГМ) предусма-тривают медикаментозное поддержание сердечно-легочных функций и противосудорожную защиту [1]. Послед ние достижения в раскрытии патофизиологи-ческих механизмов непосредственно ГИП дают опору для поиска и внедрения новых лечебных технологий. У доношенных детей основным прямым механизмом ГИП является внутриутробная асфиксия, вызванная проблемами кровообращения, в том числе в области плацентарных артерий, отслойкой плаценты или вос-палительным процессом. За этим следуют снижение объема кислорода и углекислого газа в крови и тяже-лый лактат-ацидоз. Выраженное снижение сердечного выброса в условиях гипоксии, называемое гипоксией-ишемией, в течение 12-36 ч приводит к поражению головного мозга [2].

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Cytokines and Perinatal Brain Damage

Cited by 177 publications

References 192 publications

Inhibition of Matrix Metalloproteinases-2/-9 Transiently Reduces Pre-Oligodendrocyte Loss during Lipopolysaccharide- but Not Tumour Necrosis Factor-alpha-Induced Inflammation in Fetal Ovine Glial Culture

Inhibition of Matrix Metalloproteinases-2/-9 Transiently Reduces Pre-Oligodendrocyte Loss during Lipopolysaccharide- but Not Tumour Necrosis Factor-alpha-Induced Inflammation in Fetal Ovine Glial Culture

A Review on Cerebral Palsy in Children: Bridging Ayurvedic Concepts With Scientific Approaches in Medicine

Recent Information on the Pathogenesis and Treatment of Hypoxic-Ischemic Brain Lesions in Newborns

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