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白藜芦醇通过激活 ROS 介导的 PI3K/Akt 通路减轻高糖诱导的椎间盘细胞凋亡和衰老。

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

机构信息

Department of Cosmetic Plastic Surgery, Southwest Hospital, Third Military University, Chongqing 400038, China.

Department of Orthopedic Surgery, No. 89 Hospital of PLA, Weifang, Shandong 261026, China.

出版信息

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

DOI:10.1042/BSR20171454
PMID:29273676
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5897744/
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.

摘要

背景

糖尿病与椎间盘退变密切相关。髓核（NP）细胞凋亡和衰老，是退变椎间盘的典型细胞特征。白藜芦醇是一种新发现的植物抗毒素，对软骨组织具有保护作用。

目的

探讨白藜芦醇是否可以预防高糖诱导的 NP 细胞凋亡和衰老，并研究其在这一过程中的潜在机制。

方法

将大鼠 NP 细胞分别在含 10%胎牛血清的培养基（对照组）或含 0.2 M 高葡萄糖浓度的 10%胎牛血清培养基（实验组）中培养 3 天。在实验组的培养基中加入白藜芦醇或白藜芦醇与 LY294002 的混合物，以研究白藜芦醇和 PI3K/Akt 通路的作用。

结果

与对照组相比，高葡萄糖显著促进 NP 细胞凋亡和衰老。白藜芦醇对高糖诱导的 NP 细胞凋亡和衰老具有保护作用。进一步分析表明，白藜芦醇在高糖条件下抑制活性氧（ROS）的产生，增加 PI3K/Akt 通路的活性。然而，LY294002 对高糖处理的白藜芦醇组中的 ROS 含量没有显著影响。

结论

白藜芦醇可以减轻高糖诱导的 NP 细胞凋亡和衰老，ROS 介导的 PI3K/Akt 通路的激活可能是这一过程的潜在机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/cd771b5c8a69/bsr-38-bsr20171454-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/37cb53d1919f/bsr-38-bsr20171454-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/14e86e52a469/bsr-38-bsr20171454-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/8d2f60fbf6f7/bsr-38-bsr20171454-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/cab5cbfb3580/bsr-38-bsr20171454-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/cd771b5c8a69/bsr-38-bsr20171454-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/37cb53d1919f/bsr-38-bsr20171454-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/14e86e52a469/bsr-38-bsr20171454-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/8d2f60fbf6f7/bsr-38-bsr20171454-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/cab5cbfb3580/bsr-38-bsr20171454-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a56e/5897744/cd771b5c8a69/bsr-38-bsr20171454-g5.jpg

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