Protective effect of CDDO-ethyl amide against high-glucose-induced oxidative injury via the Nrf2/HO-1 pathway
| Autor: | Jinfeng Ma, De-Chun Wang, Ting Wang, Yang Liu, Zheng-Gang Zhou, Cun-Xin Zhang |
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| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
MAPK/ERK pathway Nucleus Pulposus NF-E2-Related Factor 2 Apoptosis Context (language use) medicine.disease_cause Antioxidants 03 medical and health sciences Western blot Animals Medicine Orthopedics and Sports Medicine Oleanolic Acid Protein kinase A Cells Cultured chemistry.chemical_classification Reactive oxygen species medicine.diagnostic_test business.industry Cytoprotection Cell biology Oxidative Stress Glucose 030104 developmental biology chemistry Biochemistry Surgery Rabbits Neurology (clinical) Reactive Oxygen Species business Heme Oxygenase-1 Oxidative stress |
| Zdroj: | The Spine Journal. 17:1017-1025 |
| ISSN: | 1529-9430 |
| DOI: | 10.1016/j.spinee.2017.03.015 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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