Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.

<h4>Background</h4>Recently, several studies have reported Yokukansan (Tsumura TJ-54), a traditional Japanese medicine, as a potential new drug for the treatment of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress is known to play an important role in the pathogenesis of...

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Autores principales:	Toru Hiratsuka, Shinsuke Matsuzaki, Shingo Miyata, Mitsuhiro Kinoshita, Kazuaki Kakehi, Shinji Nishida, Taiichi Katayama, Masaya Tohyama
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2010
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9199ae2f7a49460da6d55aded088de7d
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spelling	oai:doaj.org-article:9199ae2f7a49460da6d55aded088de7d2021-11-18T07:03:26ZYokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.1932-620310.1371/journal.pone.0013280https://doaj.org/article/9199ae2f7a49460da6d55aded088de7d2010-10-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20967273/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Recently, several studies have reported Yokukansan (Tsumura TJ-54), a traditional Japanese medicine, as a potential new drug for the treatment of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress is known to play an important role in the pathogenesis of AD, particularly in neuronal death. Therefore, we examined the effect of Yokukansan on ER stress-induced neurotoxicity and on familial AD-linked presenilin-1 mutation-associated cell death.<h4>Methods</h4>We employed the WST-1 assay and monitored morphological changes to evaluate cell viability following Yokukansan treatment or treatment with its components. Western blotting and PCR were used to observe the expression levels of GRP78/BiP, caspase-4 and C/EBP homologous protein.<h4>Results</h4>Yokukansan inhibited neuronal death during ER stress, with Cnidii Rhizoma (Senkyu), a component of Yokukansan, being particularly effective. We also showed that Yokukansan and Senkyu affect the unfolded protein response following ER stress and that these drugs inhibit the activation of caspase-4, resulting in the inhibition of ER stress-induced neuronal death. Furthermore, we found that the protective effect of Yokukansan and Senkyu against ER stress could be attributed to the ferulic acid content of these two drugs.<h4>Conclusions</h4>Our results indicate that Yokukansan, Senkyu and ferulic acid are protective against ER stress-induced neuronal cell death and may provide a possible new treatment for AD.Toru HiratsukaShinsuke MatsuzakiShingo MiyataMitsuhiro KinoshitaKazuaki KakehiShinji NishidaTaiichi KatayamaMasaya TohyamaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 10, p e13280 (2010)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Toru Hiratsuka Shinsuke Matsuzaki Shingo Miyata Mitsuhiro Kinoshita Kazuaki Kakehi Shinji Nishida Taiichi Katayama Masaya Tohyama Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
description	<h4>Background</h4>Recently, several studies have reported Yokukansan (Tsumura TJ-54), a traditional Japanese medicine, as a potential new drug for the treatment of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress is known to play an important role in the pathogenesis of AD, particularly in neuronal death. Therefore, we examined the effect of Yokukansan on ER stress-induced neurotoxicity and on familial AD-linked presenilin-1 mutation-associated cell death.<h4>Methods</h4>We employed the WST-1 assay and monitored morphological changes to evaluate cell viability following Yokukansan treatment or treatment with its components. Western blotting and PCR were used to observe the expression levels of GRP78/BiP, caspase-4 and C/EBP homologous protein.<h4>Results</h4>Yokukansan inhibited neuronal death during ER stress, with Cnidii Rhizoma (Senkyu), a component of Yokukansan, being particularly effective. We also showed that Yokukansan and Senkyu affect the unfolded protein response following ER stress and that these drugs inhibit the activation of caspase-4, resulting in the inhibition of ER stress-induced neuronal death. Furthermore, we found that the protective effect of Yokukansan and Senkyu against ER stress could be attributed to the ferulic acid content of these two drugs.<h4>Conclusions</h4>Our results indicate that Yokukansan, Senkyu and ferulic acid are protective against ER stress-induced neuronal cell death and may provide a possible new treatment for AD.
format	article
author	Toru Hiratsuka Shinsuke Matsuzaki Shingo Miyata Mitsuhiro Kinoshita Kazuaki Kakehi Shinji Nishida Taiichi Katayama Masaya Tohyama
author_facet	Toru Hiratsuka Shinsuke Matsuzaki Shingo Miyata Mitsuhiro Kinoshita Kazuaki Kakehi Shinji Nishida Taiichi Katayama Masaya Tohyama
author_sort	Toru Hiratsuka
title	Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
title_short	Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
title_full	Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
title_fullStr	Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
title_full_unstemmed	Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.
title_sort	yokukansan inhibits neuronal death during er stress by regulating the unfolded protein response.
publisher	Public Library of Science (PLoS)
publishDate	2010
url	https://doaj.org/article/9199ae2f7a49460da6d55aded088de7d
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Yokukansan inhibits neuronal death during ER stress by regulating the unfolded protein response.

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