eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
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SCImago Journal & Country Rank
1/2019
vol. 15
 
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abstract:
Basic research

Stilbene glycoside protects osteoblasts against oxidative damage via Nrf2/HO-1 and NF-κB signaling pathways

Jian Cheng, Haohao Wang, Zhida Zhang, Keyong Liang

Arch Med Sci 2019; 15, 1: 192–203
Online publish date: 2018/11/28
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Introduction
Oxidative stress is currently proposed as a risk factor associated with the development and progression of osteoporosis. Here, the effect of 2,3,5,4’-tetrahydroxystilbene-2-O-β-D-glycoside (THSG) on oxidative damage was investigated in an osteoblast-like MC3T3-E1 cell model.

Material and methods
In this study, MC3T3-E1 cells were treated with hydrogen peroxide (H2O2) (100 µM) and THSG (20, 50 and 100 µM), and alkaline phosphatase (ALP). ROS and MDA levels were measured using specific kits. Meanwhile, cell viability and apoptosis were also assessed using MTT methods and flow cytometry, respectively. Then, expression levels of Nrf2 and its downstream targets were determined using real-time PCR and western blotting, as well as the apoptosis related factors, including Bax, Bcl-2, caspase-3, and caspase-9.

Results
Upon H2O2 treatment, cell viability was significantly decreased, while THSG clearly attenuated this decrease in a dose-dependent manner. Compared with the negative control, H2O2 significantly decreased ALP and increased the levels of MDA, ROS and apoptosis, while THSG markedly reversed these effects in a dose-dependent manner. Moreover, THSG was identified to reverse the elevation of caspase-3, caspase-9 and Bax and the reduction of Bcl-2 induced by H2O2. For the Nrf2 signaling pathway, THSG was also observed to attenuate the up-regulation of Nrf2, HO-1, and NQO1, and the down-regulation of NF-κB induced by H2O2.

Conclusions
THSG could significantly attenuate oxidative damage induced by H2O2 via the Nrf2/NF-κB signaling pathway, providing new insights for treatments of osteoporosis induced by oxidative injury.

keywords:

THSG, osteoblast, oxidative damage, NF-κB, Nrf2/HO-1

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