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Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress

BACKGROUND: Endoplasmic reticulum stress (ERS) is one of the main mechanisms of spinal cord injury (SCI) pathology and can affect the physiological state of neurons. Icariin (ICA), the main pharmacological component of Epimedium, can relieve the symptoms of patients with SCI and has obvious protecti...

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Autores principales: Wu, Chengjie, Yang, Guanglu, Pan, Yalan, Wang, Lei, Tu, Pengcheng, Zheng, Suyang, Guo, Yang, Ma, Yong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896365/
https://www.ncbi.nlm.nih.gov/pubmed/33607999
http://dx.doi.org/10.1186/s12906-021-03233-1
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author Wu, Chengjie
Yang, Guanglu
Pan, Yalan
Wang, Lei
Tu, Pengcheng
Zheng, Suyang
Guo, Yang
Ma, Yong
author_facet Wu, Chengjie
Yang, Guanglu
Pan, Yalan
Wang, Lei
Tu, Pengcheng
Zheng, Suyang
Guo, Yang
Ma, Yong
author_sort Wu, Chengjie
collection PubMed
description BACKGROUND: Endoplasmic reticulum stress (ERS) is one of the main mechanisms of spinal cord injury (SCI) pathology and can affect the physiological state of neurons. Icariin (ICA), the main pharmacological component of Epimedium, can relieve the symptoms of patients with SCI and has obvious protective effects on neurons through ERS. METHODS: PC12 cells were induced to differentiate into neurons by nerve growth factor and identified by flow cytometry. Cell proliferation was detected by CCK8 method, cell viability was detected by SRB assay, apoptosis was detected by flow cytometry and microstructure of ER was observed by transmission electron microscope. Western blot was used to detect the protein expression of CHOP and Grp78, and qPCR was used to detect the mRNA expression of CHOP and Grp78. RESULTS: The results of CCK8, SRB and flow cytometry showed that ICA could relieve ERS and reduce apoptosis of PC12 cells. The results of transmission microscope showed that ICA could reduce apoptosis of PC12 cells caused by ERS. The results of Western blot and q-PCR showed that ICA could inhibit ERS by down-regulating the expression of CHOP and Grp78. CONCLUSIONS: ICA can inhibit ERS and promote the repair of PC12 cells by down-regulating the expression of CHOP and Grp78. ICA has the potential to promote the recovery of spinal cord injury. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12906-021-03233-1.
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spelling pubmed-78963652021-02-22 Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress Wu, Chengjie Yang, Guanglu Pan, Yalan Wang, Lei Tu, Pengcheng Zheng, Suyang Guo, Yang Ma, Yong BMC Complement Med Ther Research Article BACKGROUND: Endoplasmic reticulum stress (ERS) is one of the main mechanisms of spinal cord injury (SCI) pathology and can affect the physiological state of neurons. Icariin (ICA), the main pharmacological component of Epimedium, can relieve the symptoms of patients with SCI and has obvious protective effects on neurons through ERS. METHODS: PC12 cells were induced to differentiate into neurons by nerve growth factor and identified by flow cytometry. Cell proliferation was detected by CCK8 method, cell viability was detected by SRB assay, apoptosis was detected by flow cytometry and microstructure of ER was observed by transmission electron microscope. Western blot was used to detect the protein expression of CHOP and Grp78, and qPCR was used to detect the mRNA expression of CHOP and Grp78. RESULTS: The results of CCK8, SRB and flow cytometry showed that ICA could relieve ERS and reduce apoptosis of PC12 cells. The results of transmission microscope showed that ICA could reduce apoptosis of PC12 cells caused by ERS. The results of Western blot and q-PCR showed that ICA could inhibit ERS by down-regulating the expression of CHOP and Grp78. CONCLUSIONS: ICA can inhibit ERS and promote the repair of PC12 cells by down-regulating the expression of CHOP and Grp78. ICA has the potential to promote the recovery of spinal cord injury. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12906-021-03233-1. BioMed Central 2021-02-19 /pmc/articles/PMC7896365/ /pubmed/33607999 http://dx.doi.org/10.1186/s12906-021-03233-1 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Wu, Chengjie
Yang, Guanglu
Pan, Yalan
Wang, Lei
Tu, Pengcheng
Zheng, Suyang
Guo, Yang
Ma, Yong
Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title_full Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title_fullStr Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title_full_unstemmed Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title_short Icariin promotes the repair of PC12 cells by inhibiting endoplasmic reticulum stress
title_sort icariin promotes the repair of pc12 cells by inhibiting endoplasmic reticulum stress
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7896365/
https://www.ncbi.nlm.nih.gov/pubmed/33607999
http://dx.doi.org/10.1186/s12906-021-03233-1
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