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

被引:19
作者
Sun, Wenshuang [1 ]
Meng, Jia [1 ]
Wang, Zhenheng [1 ]
Yuan, Tao [1 ]
Qian, Hong [1 ]
Chen, Wenxiang [1 ]
Tong, Jian [1 ]
Xie, Yu [1 ]
Zhang, Ya [1 ]
Zhao, Jianning [1 ]
Bao, Nirong [1 ]
机构
[1] Nanjing Jinling Hosp, Dept Orthoped, 305 Zhongshan East Rd, Nanjing 210000, Jiangsu, Peoples R China
关键词
MITOCHONDRIAL DYSFUNCTION; STRESS; GRAPE; PROTECTS; APOPTOSIS; THERAPY; RATS;
D O I
10.1155/2017/7529104
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
Proanthocyanidins (PCs) have shown inhibition of oxidative damage by improving Nrf-2 expression in many tissues. However, the cytoprotective effects of PCs on H2O2-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 H2O2. 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, H2O2 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 + H2O2 cotreated group. All the findings indicated that PCs could protect against the oxidative damage induced by H2O2 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.
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页数:8
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