Back to Search Start Over

Proanthocyanidins Attenuation of H2O2-Induced Oxidative Damage in Tendon-Derived Stem Cells via Upregulating Nrf-2 Signaling Pathway.

Authors :
Sun, Wenshuang
Meng, Jia
Wang, Zhenheng
Yuan, Tao
Qian, Hong
Chen, Wenxiang
Tong, Jian
Xie, Yu
Zhang, Ya
Zhao, Jianning
Bao, Nirong
Source :
BioMed Research International; 10/22/2017, Vol. 2017, p1-8, 8p
Publication Year :
2017

Abstract

Proanthocyanidins (PCs) have shown inhibition of oxidative damage by improving Nrf-2 expression in many tissues. However, the cytoprotective effects of PCs on H<subscript>2</subscript>O<subscript>2</subscript>-induced tendon damage have not been verified. The current study was aimed at assessing the cytoprotection of PCs on the oxidative cellular toxicity of tendon-derived stem cells (TDSCs) induced by H<subscript>2</subscript>O<subscript>2</subscript>. The TDSCs were isolated from patellar tendons of Sprague Dawley (SD) rats, and the cells after third passage were used for subsequent experiments. The isolated cells were identified by flow cytometry assay and multidifferentiation potential assay. Cell Counting Kit-8 assay was performed to examine cell viability. Real-Time PCR and Western Blot were employed to, respectively, assess the mRNA and protein expressions of Nrf-2, GCLM, NQO-1, and HO-1. PCs significantly improved the cell viability of TDSCs. Furthermore, H<subscript>2</subscript>O<subscript>2</subscript> upregulated Nrf-2, GCLM, NQO-1, and HO-1 without significant difference, while the proteins expressions were increased with significant difference in PCs group and PCs + H<subscript>2</subscript>O<subscript>2</subscript> cotreated group. All the findings indicated that PCs could protect against the oxidative damage induced by H<subscript>2</subscript>O<subscript>2</subscript> in TDSCs, and the cytoprotective effects might be due to the ability of PCs to activate the expressions of GCLM, HO-1, and NQO-1 via upregulating Nrf-2 signaling pathway. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
23146133
Volume :
2017
Database :
Complementary Index
Journal :
BioMed Research International
Publication Type :
Academic Journal
Accession number :
125802854
Full Text :
https://doi.org/10.1155/2017/7529104