2014Journal of Apoplexy and Nervous DiseasesRequires access

Progesterone reduce hypoxic-ischemic brain injury in neonatal rats through PI3K/Akt signaling pathway

LI Xiao-jua

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Abstract

Objective To investigate progesterone reducing hypoxic-ischemic brain injury in neonatal rats through PI3 K /Akt signaling pathway. Methods 7 days old newborn Wistar rats were randomly divided into four groups,sham group: only with neck incision,without hypoxic-ischemic treatment; model group: with neck incision and hypoxic-ischemic treatment; progsterone group: with hypoxic-ischemic treatment and 8 mg /kg progesterone was injected intraperitoneally 30 min before hypoxia,inhibitor group: 30 min before the establishment of HIBD model,16 μg /kg wortmannin was injected in the left hippocampus. Neuronal changes of hypoxic-ischemic brain were observed under electron microscopy. Protein expressions of pAkt and NF-κB in hippocampus were detected by immunohistochemistry and western blot. Results The neuronal structures in the sham group after hypoxic-ischemic for 24 hours were normal. The neuronal structures in the model group had cavitation changes and the damage reduced after being given progesterone. Inhibitor application increased hypoxic-ischemic neuronal damage. Protein expressions of pAkt decreased and NF-κB increased after hypoxic-ischemic. Progesterone pretreatment could increase pAkt and reduce NF-κB expression. The inhibitor could reduce pAkt and increase NF-κB expression. Conclusion Through activation of PI3 K /Akt signaling pathway,progesterone increase pAkt and decrease NF-κB,reduce the inflammation injury of hypoxic-ischemic brain and play a neuroprotective role in the brain.

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Objective To investigate progesterone reducing hypoxic-ischemic brain injury in neonatal rats through PI3 K /Akt signaling pathway. Methods 7 days old newborn Wistar rats were randomly divided into four groups,sham group: only with neck incision,without hypoxic-ischemic treatment; model group: with neck incision and hypoxic-ischemic treatment; progsterone group: with hypoxic-ischemic treatment and 8 mg /kg progesterone was injected intraperitoneally 30 min before hypoxia,inhibitor group: 30 min before the establishment of HIBD model,16 μg /kg wortmannin was injected in the left hippocampus. Neuronal changes of hypoxic-ischemic brain were observed under electron microscopy. Protein expressions of pAkt and NF-κB in hippocampus were detected by immunohistochemistry and western blot. Results The neuronal structures in the sham group after hypoxic-ischemic for 24 hours were normal. The neuronal structures in the model group had cavitation changes and the damage reduced after being given progesterone. Inhibitor application increased hypoxic-ischemic neuronal damage. Protein expressions of pAkt decreased and NF-κB increased after hypoxic-ischemic. Progesterone pretreatment could increase pAkt and reduce NF-κB expression. The inhibitor could reduce pAkt and increase NF-κB expression. Conclusion Through activation of PI3 K /Akt signaling pathway,progesterone increase pAkt and decrease NF-κB,reduce the inflammation injury of hypoxic-ischemic brain and play a neuroprotective role in the brain.

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Available abstract

Objective To investigate progesterone reducing hypoxic-ischemic brain injury in neonatal rats through PI3 K /Akt signaling pathway. Methods 7 days old newborn Wistar rats were randomly divided into four groups,sham group: only with neck incision,without hypoxic-ischemic treatment; model group: with neck incision and hypoxic-ischemic treatment; progsterone group: with hypoxic-ischemic treatment and 8 mg /kg progesterone was injected intraperitoneally 30 min before hypoxia,inhibitor group: 30 min before the establishment of HIBD model,16 μg /kg wortmannin was injected in the left hippocampus. Neuronal changes of hypoxic-ischemic brain were observed under electron microscopy. Protein expressions of pAkt and NF-κB in hippocampus were detected by immunohistochemistry and western blot. Results The neuronal structures in the sham group after hypoxic-ischemic for 24 hours were normal. The neuronal structures in the model group had cavitation changes and the damage reduced after being given progesterone. Inhibitor application increased hypoxic-ischemic neuronal damage. Protein expressions of pAkt decreased and NF-κB increased after hypoxic-ischemic. Progesterone pretreatment could increase pAkt and reduce NF-κB expression. The inhibitor could reduce pAkt and increase NF-κB expression. Conclusion Through activation of PI3 K /Akt signaling pathway,progesterone increase pAkt and decrease NF-κB,reduce the inflammation injury of hypoxic-ischemic brain and play a neuroprotective role in the brain.

Key concepts: Wortmannin, Neuroprotection, Medicine, PI3K/AKT/mTOR pathway, Protein kinase B, Hypoxia (environmental), Western blot, Immunohistochemistry

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