Abstract Title:

Ferulic acid ameliorates cerebral infarction by activating Akt/mTOR/4E‑BP1/Bcl‑2 anti‑apoptotic signaling in the penumbral cortex following permanent cerebral ischemia in rats.

Abstract Source:

Mol Med Rep. 2019 Feb ;19(2):792-804. Epub 2018 Dec 11. PMID: 30569126

Abstract Author(s):

Chin-Yi Cheng, Shung-Te Kao, Yu-Chen Lee

Article Affiliation:

Chin-Yi Cheng


The aim of the present study was to determine the effects of ferulic acid (FerA) administered immediately following the onset of permanent middle cerebral artery occlusion (MCAo) and then 7 days of ischemia, and also to explore the involvement of protein kinase B (Akt)‑induced signaling in the penumbral cortex. Immediately following the onset of MCAo, FerA was intravenously administered to rats at a dose of 60 mg/kg (FerA‑60 mg), 80 mg/kg (FerA‑80 mg), or 100 mg/kg (FerA‑100 mg). FerA‑80 mg and FerA‑100 mg effectively ameliorated cerebral infarction and neurological deficits 7 days following permanent cerebral ischemia. FerA‑80 mg and FerA‑100 mg significantly upregulated the expression of phospho‑Akt (p‑Akt), phospho‑mammalian target of rapamycin (p‑mTOR), and eukaryotic initiation factor 4E (eIF4E)‑binding protein 1 (4E‑BP1), and the phospho‑4E‑BP1 (p‑4E‑BP1)/4E‑BP1 and mitochondrial Bcl‑2/Bax ratios, and markedly downregulated the levels of cytochrome c‑, cleaved caspase‑3‑, and terminal deoxynucleotidyl transferase‑mediated dUTP‑biotin nick‑end labeling‑immunoreactive cells in the penumbral cortex at 7 days post‑ischemia. LY294002, a selective inhibitor of phosphoinositide 3‑kinase/Akt signaling, was administered 30 min prior to ischemia, which abrogated the upregulating effects of FerA‑100 mg on the expression of p‑Akt, p‑mTOR, 4E‑BP1, p‑4E‑BP1 and eIF4E, the mitochondrial Bcl‑2/Bax ratio and the ameliorating effect of FerA‑100 mg on cerebral infarction. FerA administered at doses of 80 and 100 mg/kg exerted beneficial effects against cerebral ischemia by activating Akt‑induced signaling. The effects of FerA at doses of 80 and 100 mg/kg on mitochondrial B‑cell lymphoma-2 (Bcl‑2)‑associated X protein‑related apoptosis were attributed to the activation of Akt/mTOR/4E‑BP1/Bcl‑2 anti‑apoptotic signaling, and eventually contributed to suppression of the cytochrome c/caspase‑3 activation pathway in the penumbral cortex 7 days following permanent cerebral ischemia.

Study Type : Animal Study

Print Options

Key Research Topics

Sayer Ji
Founder of GreenMedInfo.com

Subscribe to our informative Newsletter & get Nature's Evidence-Based Pharmacy

Our newsletter serves 500,000 with essential news, research & healthy tips, daily.

Download Now

500+ pages of Natural Medicine Alternatives and Information.

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2022 GreenMedInfo.com, Journal Articles copyright of original owners, MeSH copyright NLM.