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. 2018 Apr 13;38(2):BSR20171454.
doi: 10.1042/BSR20171454. Print 2018 Apr 27.

Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway

Wenping Wang  1 , Pei Li  2 , Jiagang Xu  3 , Xiangkun Wu  4 , Zhiliang Guo  1 , Lijing Fan  5 , Ruipeng Song  6 , Jianli Wang  7 , Li Wei  8 , Haijun Teng  7
Affiliations

Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway

Wenping Wang et al. Biosci Rep. .

Retraction in

Abstract

Background: Diabetes mellitus is closely correlated with disc degeneration. Nucleus pulposus (NP) cell apoptosis and senescence are typical cellular features within the degenerative disc. Resveratrol is a newly identified phytoalexin that has protective effects on cartilaginous tissue.

Objective: To investigate the whether resveratrol can protect against high glucose-induced NP cell apoptosis and senescence, and the potential mechanism in this process.

Methods: Rat NP cells were cultured in either 10% FBS culture medium (control group) or 10% FBS with a high glucose concentration (0.2 M, experiment group) for 3 days. Resveratrol or the combination of resveratrol and LY294002 was added into the culture medium of experiment group to investigate the effects of resveratrol and the PI3K/Akt pathway.

Results: High glucose significantly promoted NP cell apoptosis and NP cell senescence compared with the control group. Resveratrol exhibited protective effects against high glucose-induced NP cell apoptosis and senescence. Further analysis showed that resveratrol suppressed reactive oxygen species (ROS) generation and increased the activity of the PI3K/Akt pathway under the high glucose condition. However, the LY294002 had no significant effects on ROS content in the resveratrol-treated high glucose group.

Conclusion: Resveratrol can attenuate high glucose-induced NP cell apoptosis and senescence, and the activation of ROS-mediated PI3K/Akt pathway may be the potential mechanism in this process.

Keywords: apoptosis; glucose; intervertebral disc degeneration; nucleus pulposus; resveratrol; senescence.

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Conflict of interest statement

The authors declare that there are no competing interests associated with the manuscript.

Figures

Figure 1
Figure 1. Evaluation of nucleus pulposus (NP) apoptosis
(A) Flow cytometry analysis of NP cell apoptosis. (B) Caspase-3 activity measurement. Data are presented as mean ± SD (n=3); * indicates a significant difference (P<0.05) between two groups.
Figure 2
Figure 2. Evaluation of nucleus pulposus (NP) senescence
(A) SA-β-Gal staining assay and its quantification. (B) Quantification of cell cycle phases. (C) Telomerase activity measurement. Data are presented as mean ± SD (n=3); * indicates a significant difference (P<0.05) between two groups.
Figure 3
Figure 3. Real-time PCR analysis of apoptosis-related molecules and senescence markers
(A) Gene expression of the apoptosis-related molecules (Bcl-2, Bax, and caspase-3). (B) Gene expression of the senescence markers (p16 and p53). Data are presented as mean ± SD (n=3); * indicates a significant difference (P<0.05) between two groups.
Figure 4
Figure 4. Intracellular reactive oxygen species (ROS) content measurement
Data are presented as mean ± SD (n=3); * indicates a significant difference (P<0.05) between two groups.
Figure 5
Figure 5. Western blotting analysis of PI3K/Akt pathway activity
Data are presented as mean ± SD (n=3); * indicates a significant difference (P<0.05) between two groups.
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