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Updated: Jul 18, 2026
Screening Assay for Oxidative Stress in a Feline Astrocyte Cell Line, G355-5
Published on: July 13, 2011
Protective effect of CDDO-ethyl amide against high-glucose-induced oxidative injury via the Nrf2/HO-1 pathway
Cun-Xin Zhang1, Ting Wang2, Jin-Feng Ma2
1Qingdao Spine Center, Qingdao Municipal Hospital, Qingdao University, 5# Donghai Rd, Shinan District, Qingdao 266061, China.
Background Context:
Intervertebral disc degeneration (IDD) is the main cause of low back pain, and nucleus pulposus (NP) cell apoptosis is an important risk factor of IDD. However, the molecular mechanism of this disease remains unknown.
Purpose:
To assess the potential protective effect of CDDO-ethyl amide (EA) against high-glucose-induced oxidative stress injury in NP cells and to investigate the mechanism of antioxidative effects and apoptotic inhibition.
Study Design/Setting:
To find new molecule to inhibit intervertebral disc degeneration.
Methods:
Viability, reactive oxygen species (ROS) levels, and apoptosis were examined in NP cells. The protein expression levels of HO-1 and Nrf2 were measured through Western blot RESULTS: CDDO-EA elicited cytoprotective effects against NP cell apoptosis and ROS accumulation induced by high glucose. CDDO-EA treatment increased the HO-1 and Nrf2 expression abrogated by HO-1, Nrf2, and mitogen-activated protein kinase inhibitors.
Conclusions:
The phosphorylation and nuclear translocation of Nrf2 are crucial for HO-1 overexpression induced by CDDO-EA, which is essential for the cytoprotection against high-glucose-induced oxidative stress in NP cells.
