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FEBS Open Bio. 2019 Oct 12. doi: 10.1002/2211-5463.12742. [Epub ahead of print]

NGF protects neuroblastoma cells against β-amyloid-induced apoptosis via the Nrf2/HO-1 pathway.

Author information

1
Department of Neurosurgery, Luoyang Central Hospital Affiliated to Zhengzhou University, China.
2
Department of Intensive Care Unit, Sir Run Run Shaw Hospital Affiliated by Zhejiang University School of Medicine, Hangzhou, China.
3
Department of Anesthesia Surgery, Sanmenxia Central Hospital, China.

Abstract

As one of the main neurotrophic factors, nerve growth factor (NGF) participates in various processes related to viability, plasticity, and neuronal growth. NGF is known to protect against cell death and toxicity triggered by β-amyloid (Aβ), but the underlying mechanism remains unclear. Here, we investigated this process in SKNSH neuroblastoma, in which NGF reduced cell death induced by Aβ25-35. Furthermore, NGF suppressed the production of reactive oxygen species (ROS) and promoted antioxidant function via Aβ25-35. Additionally, we demonstrated that NGF impaired the activation of the JNK/c-Jun signaling pathway and significantly increased Nrf2 nuclear translocation and HO-1 expression. Nrf2 elimination abolished the protective effect of NGF-1 on Aβ25-35-induced ROS generation, apoptosis, and activation of the JNK/c-Jun pathway. The results of our study indicate that NGF protects neuroblastoma against injury triggered by Aβ25-35 via suppression of ROS-JNK/c-Jun pathway stimulation through the Nrf2/HO-1 pathway.

KEYWORDS:

JNK/c-Jun; NGF; Nrf2; apoptosis; β-amyloid

PMID:
31605506
DOI:
10.1002/2211-5463.12742
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