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Mol Med Rep. 2019 May 30. doi: 10.3892/mmr.2019.10312. [Epub ahead of print]

Forsythiaside A protects against focal cerebral ischemic injury by mediating the activation of the Nrf2 and endoplasmic reticulum stress pathways.

Author information

1
Department of Neurology, Xintai Municipal People's Hospital, Xintai, Shandong 271200, P.R. China.
2
Department of Neurology, The First Hospital of Xi'an, Xi'an, Shaanxi 710002, P.R. China.
3
Department of Neurology, Cangzhou People's Hospital, Cangzhou, Hebei 061000, P.R. China.

Abstract

Ischemic stroke is a common type of stroke with a high mortality and morbidity rate. Preventing and controlling cerebral ischemic injury is particularly important. Forsythiaside A (FA) has been reported to have anti‑inflammatory and antioxidant activities. The aim of the present study was to explore the impact of FA on middle cerebral artery occlusion (MCAO)‑induced cerebral ischemic injury in rats. The results indicated that FA markedly increased the percent survival and decreased the neurological deficit score in rats with cerebral ischemic injury. Furthermore, cell apoptosis was significantly inhibited by FA administration, which was accompanied by decreased caspase‑3 and caspase‑9 expression. A marked increase in the expression levels of nuclear factor‑erythroid 2‑related factor 2 (Nrf2), NAD(P)H quinone dehydrogenase 1 and glutathione‑s‑transferase was detected in FA‑treated rats. In addition, treatment with FA reduced malonaldehyde expression, and enhanced the expression of superoxide dismutase and glutathione. Furthermore, endoplasmic reticulum (ER) stress was vastly alleviated by FA treatment, as evidenced by the increased expression of B‑cell lymphoma 2, apoptosis regulator and the downregulated expression of phosphorylated (phospho)‑protein kinase RNA‑like ER kinase (PERK)/PERK, phospho‑inositol‑requiring enzyme 1 (IRE1α)/IRE1α and CCAAT‑enhancer‑binding proteins homologous protein. Taken together, the present study demonstrated that FA attenuated cerebral ischemic damage via mediation of the activation of Nrf2 and ER stress pathways. These data may provide ideas for novel treatment strategies of cerebral ischemic damage.

PMID:
31173213
DOI:
10.3892/mmr.2019.10312

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