Effects of activated protein C on neonatal hypoxic ischemic brain injury

Yesilirmak, Didem Cemile; Kumral, Abdullah; Tugyan, Kazim; Cilaker, Serap; Baskın, Hüseyin; Yılmaz, Osman; Duman, Nuray; Özkan, Hasan

doi:10.1016/j.brainres.2008.02.088

Cited by 26 publications

(20 citation statements)

References 39 publications

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“…Studies have demonstrated that the 7-day-old rodent has the analogous brain maturity to model a third-trimester human fetus (Kim et al, 2008;Yesilirmak et al, 2008). Despite the fact that perinatal asphyxia closely corresponds to experimental models of cerebral HI, no reliable treatment strategies have been introduced to mitigate neurological injury and the resulting impairments in the clinical setting.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Zhu¹,

L²,

Guo³

et al. 2011

Genet. Mol. Res.

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ABSTRACT. The hypoxic-ischemic encephalopathy caused by peripartum asphyxia is a serious disease in newborn infants, and effective therapies need to be developed to reduce injury-related disorders. We evaluated the effects of NEP1-40 and fasudil on Nogo-A expression in neonatal hypoxic-ischemic brain damage (HIBD) rats. Seven-day-old Wistar rats were randomly divided into control, HIBD, NEP1-40, and fasudil groups. NEP1-40 and fasudil groups were injected intraperitoneally with these compounds. Rat brains at 6, 24, 72 h, and 7 days after HIBD were collected to determine histopathological damage and the expression levels of Nogo-A. Histopathological damage was reduced in NEP1-40 and fasudil groups compared with the untreated HIBD group. The expression of Nogo-A in the HIBD group was significantly higher than that in control, NEP1-40 and fasudil groups at the same times. Compared with the fasudil group, the expression levels of Nogo-A were significantly reduced in the NEP1-40 group. We conclude that NPE1-40 and fasudil have potential for neuroprotective effects in the neonatal rat HIBD model, mediated by inhibiting Nogo-A/ Rho pathways.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Zhu¹,

L²,

Guo³

et al. 2011

Genet. Mol. Res.

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show abstract

“…'nın (27) (27) Yeşilırmak ve ark. (28) deneysel olarak hipoksik iskemik beyin hasarı oluşturulan neonatal ratlarda APC'nin antiapopitotik etkiyle nöron kaybını azalttığını bildirmiştir.…”

Section: Grup Apc 30unclassified

Neuroprotective Efficacy of Activated Protein C in An Experimental Spinal Cord Injury Model in Rats

Polat¹,

Gökmen²,

Öçmen³

et al. 2012

JTAICS

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“…Group 2 (n = 7) pups were given physiologic saline (0.2 mL) by intraperitoneal injection. Group 3 (n = 7) pups were treated with 0.2 mg/kg per day APC by intraperitoneal injection 3 times a week for 2 weeks (on days 1, 3, 5, 8, 10, and 12 of life) [18]. On the 15th day of life, the rat pups were subjected to hypoxia (groups 2 and 3) in an airtight Plexiglas chamber perfused with 100% carbon dioxide for 5 minutes.…”

Section: Experimental Designmentioning

confidence: 99%

“…For establishing apoptotic index, 1000 cells were counted in ileum. Cells showing apoptotic morphology were given as percentile [18].…”

Section: In Situ Cell Death Detectionmentioning

confidence: 99%

Activated protein C reduces intestinal injury in an experimental model of necrotizing enterocolitis

Kumral

Yesilirmak

Tugyan

et al. 2010

Journal of Pediatric Surgery

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Effects of activated protein C on neonatal hypoxic ischemic brain injury

Cited by 26 publications

References 39 publications

Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Neuroprotective effects of NEP1-40 and fasudil on Nogo-A expression in neonatal rats with hypoxic-ischemic brain damage

Neuroprotective Efficacy of Activated Protein C in An Experimental Spinal Cord Injury Model in Rats

Activated protein C reduces intestinal injury in an experimental model of necrotizing enterocolitis

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