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Acorus calamus extract and its component α-asarone attenuate murine hippocampal neuronal cell death induced by l-glutamate and tunicamycin
Author(s) -
Masashi Mikami,
Takuya Ohba,
Yuta Yoshino,
Shinsuke Nakamura,
Kenichi Ito,
Hiroyuki Kojima,
Tatsuji Takahashi,
Arunasiri Iddamalgoda,
Shintaro Inoue,
Masamitsu Shimazawa,
Hideaki Hara
Publication year - 2021
Publication title -
bioscience biotechnology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.509
H-Index - 116
eISSN - 1347-6947
pISSN - 0916-8451
DOI - 10.1093/bbb/zbaa071
Subject(s) - acorus calamus , tunicamycin , oxidative stress , reactive oxygen species , calamus , endoplasmic reticulum , programmed cell death , biology , unfolded protein response , chemistry , pharmacology , microbiology and biotechnology , biochemistry , botany , apoptosis , rhizome
The Asian traditional medicinal plant Acorus calamus and its component α-asarone exhibited various biological activities, such as antiinflammation and antioxidant effects. In the present study, we investigated the in vitro effects of A. calamus extract and α-asarone on oxidative stress- and endoplasmic reticulum (ER) stress–induced cell death in hippocampal HT22 cells. A. calamus extract and α-asarone both significantly suppressed cell death induced by the oxidative stress inducer l-glutamate and ER stress inducer tunicamycin. A. calamus extract and α-asarone also significantly reduced reactive oxygen species (ROS) production induced by l-glutamate. Moreover, A. calamus extract and α-asarone suppressed the phosphorylation of protein kinase RNA-like ER kinase (PERK) induced by tunicamycin. These results suggest that A. calamus extract and α-asarone protect hippocampal cells from oxidative stress and ER stress by decreasing ROS production and suppressing PERK signaling, respectively. α-Asarone has potential as a potent therapeutic candidate for neurodegenerative diseases, including Alzheimer's disease.

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