Aloperine activates the Nrf2‑ARE pathway when ameliorating early brain injury in a subarachnoid hemorrhage model Corrigendum in /10.3892/etm.2024.12552

Song,Shibin; Chen,Yimin; Han,Feng; Dong,Minghao; Xiang,Xin; Sui,Jianmei; Li,Yuming; Yang,Hua; Liu,Jian

doi:10.3892/etm.2018.5896

Aloperine activates the Nrf2‑ARE pathway when ameliorating early brain injury in a subarachnoid hemorrhage model

Corrigendum in: /10.3892/etm.2024.12552

Authors:
- Shibin Song
- Yimin Chen
- Feng Han
- Minghao Dong
- Xin Xiang
- Jianmei Sui
- Yuming Li
- Hua Yang
- Jian Liu
View Affiliations

Affiliations: Department of Neurosurgery, Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou 550004, P.R. China
Published online on: February 26, 2018 https://doi.org/10.3892/etm.2018.5896
Pages: 3847-3855
Copyright: © Song et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Aloperine (ALO) exhibits neuroprotective effects against oxidative stress in vitro; however, its protective effect in early brain injury (EBI) following experimental subarachnoid hemorrhage (SAH) remains to be elucidated. The aim of the current study was to evaluate the antioxidant activity of ALO in EBI, and its association with nuclear factor erythroid‑related factor 2 and the antioxidant responsive element (Nrf2‑ARE) survival pathway. In the present study, an experimental SAH model was induced in rats following a prechiasmatic cistern injection. All rats were randomly divided into five groups: Sham, SAH, SAH+ vehicle, and an SAH+ ALO group (including low and high doses). ALO was administrated intraperitoneally at 2 and 24 h following induction of the SAH model. Brain samples were collected from each group at 48 h after SAH induction. Subsequently, western blotting, immunohistochemistry and cell apoptosis assays were performed, along with assessments for brain edema, neurological deficit, and the activity of oxidant/antioxidant factors. It was observed that the expression of Nrf2‑ARE pathway‑associated agents, including Nrf2, and heme oxygenase‑1, were markedly increased in the high concentration ALO group compared with that of the SAH group. In addition, the level of oxidative damage was reduced. Furthermore, early brain damage, including brain edema, neurological deficit and cellular apoptosis were significantly ameliorated. In conclusion, the results of the present study indicate that ALO can ameliorate oxidative damage against EBI following SAH, most likely via the Nrf2‑ARE survival pathway.

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