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Article Publish Status: FREE
Abstract Title:

Protective effects of ginsenoside Rg3 on TNF-α-induced human nucleus pulposus cells through inhibiting NF-κB signaling pathway.

Abstract Source:

Life Sci. 2019 Jan 1 ;216:1-9. Epub 2018 Nov 11. PMID: 30428306

Abstract Author(s):

Jiang Chen, Gen-Zhe Liu, Qi Sun, Fan Zhang, Chu-Yin Liu, Lin Yuan, Xue-Qian Zhao, Yong-Jun Wang, Yu-Song Jia

Article Affiliation:

Jiang Chen

Abstract:

This work aims to evaluate the effect of ginsenoside Rg3 on the apoptosis, proliferation, extracellular matrix (ECM) metabolism and oxidative stress-induced damage of human nucleus pulposus cells (NPCs) induced by TNF-α. The human NPCs were divided into Control, TNF-α, TNF-α + low Rg3, TNF-α + medium Rg3 and TNF-α + high Rg3 groups. Annexin V-FITC/PI, CCK-8 and flow cytometry were used to detect the apoptosis, proliferation, and cell cycle of NPCs, respectively. The expressions of ECM-related molecules were determined by qRT-PCR, ELISA and Western blotting. NF-κB p65 pathway and apoptosis-related proteins were evaluated by Western blotting, and the production of reactive oxygen species (ROS) was detected by DCFH-DA assay. Compared with Control group, NPCs in the TNF-α group had elevated proportion of apoptotic cells with up-regulation of Bax and Caspase-3 and down-regulation of Bcl-2. Besides, TNF-α inhibited proliferation and arrested cell cycle at G1 of NPCs. Moreover, human NPCs induced by TNF-α presented the increase in the expressions of ECM degrading genes (MMP3 and ADAMTS5), the content of ROS and malondialdehyde (MDA), and the expression of NF-κB/p65 in nucleus, but showed the decrease in the expression of ECM synthesis genes (Aggrecan and COL2A1) and the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX). However, NPCs treated by both TNF-αand Rg3 demonstrated a certain degree of reversal in the above indexes, which became increasingly evident with the up-regulation of Rg3 concentration. Ginsenoside Rg3 may exert the effect of attenuating TNF-α-induced NPCs impairment via blocking the NF-κB signaling pathway.

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