Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis

Pectolinarin, [5,7-Dihydroxy 4′,6-dimethoxyflavone 7-rutinoside, 7-[[6-O-(6-Deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl] oxy]-5-hydroxy-6-methoxy-2-(4-ethoxyphenyl)-4H-1-benzopyran-4-one], has been stated one of the major compounds in Cirsium nipponicum (Maxim.) Makino. It is characterized by biolo...

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Main Authors: Ji-Hye Song, Kisang Kwon, O-Yu Kwon, Eun-Ryeong Lee, Seung-Whan Kim, Kyung-Hee Kang
Format: Article
Language:English
Published: Frontiers Media S.A. 2020-09-01
Series:Frontiers in Public Health
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fpubh.2020.00478/full
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author Ji-Hye Song
Kisang Kwon
O-Yu Kwon
Eun-Ryeong Lee
Seung-Whan Kim
Kyung-Hee Kang
author_facet Ji-Hye Song
Kisang Kwon
O-Yu Kwon
Eun-Ryeong Lee
Seung-Whan Kim
Kyung-Hee Kang
author_sort Ji-Hye Song
collection DOAJ
description Pectolinarin, [5,7-Dihydroxy 4′,6-dimethoxyflavone 7-rutinoside, 7-[[6-O-(6-Deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl] oxy]-5-hydroxy-6-methoxy-2-(4-ethoxyphenyl)-4H-1-benzopyran-4-one], has been stated one of the major compounds in Cirsium nipponicum (Maxim.) Makino. It is characterized by biological functions of hepatoprotective, anti-inflammatory and antiobesity activities. In this research, it was explained that pectolinarin causes apoptosis in PC12 cells conducted by DNA fragmentation and formation on apoptotic bodies through the activation of ER stress sensors (ATF6 fragmentation and eIF2α phosphorylation). The result of treating the PC12 cells with 50 μM pectolinarin for 24 h has come to increase ATF6 mRNA expression up to 1.6 times, PERK expression up to 1.7 times and IRE1 expression up to 1.4 times, respectively, compared to those of the control. ATF6 fragmentation by pectolinarin treatment was increased about 2 times compared with its control, and phosphorylation of eIF2α was increased 2.5 times. The results proposed that the perception of the molecular mechanisms underlying pectolinarin-caused apoptosis may be useful in new natural medicinal products and health supplements for the apoptosis-related diseases.
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spelling doaj.art-e83c3d044458493b83ee9ab8a43cc0582022-12-22T01:54:47ZengFrontiers Media S.A.Frontiers in Public Health2296-25652020-09-01810.3389/fpubh.2020.00478571690Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced ApoptosisJi-Hye Song0Kisang Kwon1O-Yu Kwon2Eun-Ryeong Lee3Seung-Whan Kim4Kyung-Hee Kang5Departments of Anatomy and Cell Biology, College of Medicine, Chungnam National University, Daejeon, South KoreaDepartments of Anatomy and Cell Biology, College of Medicine, Chungnam National University, Daejeon, South KoreaDepartments of Anatomy and Cell Biology, College of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Biomedical Laboratory Science, College of Health and Welfare, Kyungwoon University, Gumi, South KoreaDepartment of Emergency Medicine, College of Medicine, Chungnam National University, Daejeon, South KoreaDepartment of Dental Hygiene, College of Medical Science, Konyang University, Daejeon, South KoreaPectolinarin, [5,7-Dihydroxy 4′,6-dimethoxyflavone 7-rutinoside, 7-[[6-O-(6-Deoxy-α-L-mannopyranosyl)-β-D-glucopyranosyl] oxy]-5-hydroxy-6-methoxy-2-(4-ethoxyphenyl)-4H-1-benzopyran-4-one], has been stated one of the major compounds in Cirsium nipponicum (Maxim.) Makino. It is characterized by biological functions of hepatoprotective, anti-inflammatory and antiobesity activities. In this research, it was explained that pectolinarin causes apoptosis in PC12 cells conducted by DNA fragmentation and formation on apoptotic bodies through the activation of ER stress sensors (ATF6 fragmentation and eIF2α phosphorylation). The result of treating the PC12 cells with 50 μM pectolinarin for 24 h has come to increase ATF6 mRNA expression up to 1.6 times, PERK expression up to 1.7 times and IRE1 expression up to 1.4 times, respectively, compared to those of the control. ATF6 fragmentation by pectolinarin treatment was increased about 2 times compared with its control, and phosphorylation of eIF2α was increased 2.5 times. The results proposed that the perception of the molecular mechanisms underlying pectolinarin-caused apoptosis may be useful in new natural medicinal products and health supplements for the apoptosis-related diseases.https://www.frontiersin.org/article/10.3389/fpubh.2020.00478/fullpectolinarinPC12 cellsendoplasmic reticulum (ER)stresssensor
spellingShingle Ji-Hye Song
Kisang Kwon
O-Yu Kwon
Eun-Ryeong Lee
Seung-Whan Kim
Kyung-Hee Kang
Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
Frontiers in Public Health
pectolinarin
PC12 cells
endoplasmic reticulum (ER)
stress
sensor
title Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
title_full Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
title_fullStr Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
title_full_unstemmed Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
title_short Impact of Endoplasmic Reticulum Stress Sensors on Pectolinarin Induced Apoptosis
title_sort impact of endoplasmic reticulum stress sensors on pectolinarin induced apoptosis
topic pectolinarin
PC12 cells
endoplasmic reticulum (ER)
stress
sensor
url https://www.frontiersin.org/article/10.3389/fpubh.2020.00478/full
work_keys_str_mv AT jihyesong impactofendoplasmicreticulumstresssensorsonpectolinarininducedapoptosis
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AT oyukwon impactofendoplasmicreticulumstresssensorsonpectolinarininducedapoptosis
AT eunryeonglee impactofendoplasmicreticulumstresssensorsonpectolinarininducedapoptosis
AT seungwhankim impactofendoplasmicreticulumstresssensorsonpectolinarininducedapoptosis
AT kyungheekang impactofendoplasmicreticulumstresssensorsonpectolinarininducedapoptosis