Inhibition of endoplasmic reticulum stress is involved in the neuroprotective effect of aFGF in neonatal hypoxic-ischaemic brain injury
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Yingying Hu1,*, Zhouguang Wang2,*, Shulin Pan1, Mingchu Fang1, Huai Jiang1, Yuqin Mao2, Hao Zhang1, Yiming Ji3, Fabiao Zhang3, Li Lin2, Zhenlang Lin1 and Jian Xiao2
1Department of Neonatology, The Second Affiliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325027, China
2Molecular Pharmacology Research Center, School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou, Zhejiang, 325035, China
3Department of Hepatobiliary Surgery, Taizhou Hospital of Zhejiang Province, Wenzhou Medical University, Linhai, 317000, China
*These authors contributed equally to this work
Li Lin, email: firstname.lastname@example.org
Zhenlang Lin, email: email@example.com
Jian Xiao, email: firstname.lastname@example.org
Keywords: acidic fibroblast growth factor, neonatal hypoxic-ischaemic brain injury, endoplasmic reticulum stress, intranasal
Received: January 23, 2017 Accepted: April 11, 2017 Published: April 29, 2017
Acidic fibroblast growth factor (aFGF) has been shown to exert neuroprotective effects in experimental models and human patients. In this study, we investigated whether aFGF intranasal-treatment protected against neonatal hypoxic-ischaemic brain injury and evaluated the role of endoplasmic reticulum stress. The Rice-Vannucci model of neonatal hypoxic-ischaemic brain injury was used in 7-day-old rats, which were subjected to unilateral carotid artery ligation followed by 2.5 h of hypoxia. Intranasal aFGF or vehicle was administered immediately after hypoxic-ischaemic injury (100 ng/g) and then twice a day for 1 week to evaluate the long-term effects. Here we reported that intranasal-treatment with aFGF significantly reduced hypoxic-ischaemic brain infarct volumes and the protective effects were at least partially via inhibiting endoplasmic reticulum stress. In addition, aFGF exerted long-term neuroprotective effects against brain atrophy and neuron loss at 7-day after injury. Our data indicate that therapeutic strategies targeting endoplasmic reticulum stress may be promising to the treatment of neonatal hypoxic-ischaemic brain injury.
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