Open AccessAtrial natriuretic peptide protects vertebral endplate chondrocytes against H2O2‑induced apoptosis and oxidative stress through activation of the Nrf2/HO‑1 signaling pathway
Author(s) -
Feiping He,
Jingying Gai,
Jun Wang,
Lei Tang,
Yifeng Liu,
Qingchun Feng
Publication year - 2021
Publication title -
molecular medicine reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.727
H-Index - 56
eISSN - 1791-3004
pISSN - 1791-2997
DOI - 10.3892/mmr.2021.12394
Subject(s) - oxidative stress , apoptosis , superoxide dismutase , signal transduction , atrial natriuretic peptide , viability assay , microbiology and biotechnology , chemistry , malondialdehyde , intracellular , medicine , endocrinology , biology , biochemistry
The present study aimed to investigate the effect of atrial natriuretic peptide (ANP) on cell apoptosis and oxidative stress in H 2 O 2 ‑induced vertebral endplate chondrocytes (EPCs), and to assess the associated mechanisms involved. Cell viability and apoptosis were evaluated using the Cell Counting Kit‑8 method and TUNEL assay, respectively. In addition, the scavenging capability was detected using various enzymatic assays, and the quantity of nitric oxide (NO) and malondialdehyde (MDA), and activity of superoxide dismutase (SOD) were assessed. The expression levels of apoptosis‑related proteins, activation of the nuclear factor erythroid 2‑related factor 2 (Nrf2)/heme oxygenase‑1 (HO‑1) signaling pathway induced by H 2 O 2 and the effect of treatment with ANP on vertebral EPCs were detected by western blotting. The results revealed that ANP protected EPCs from H 2 O 2 ‑induced cell damage. H 2 O 2 ‑induced intracellular MDA was decreased by ANP, and the levels of SOD and NO were increased in the presence of ANP. ANP also inhibited the H 2 O 2 ‑induced alterations in the expression levels of cleaved‑caspase‑3, Bax and Bcl‑2. Finally, ANP blocked H2O2‑induced oxidative stress through activating the Nrf2/HO‑1 signaling pathway. These findings suggested that ANP may effectively protect EPCs through inhibition of H 2 O 2 ‑induced oxidant injury and cell death by activating the Nrf2/HO‑1 signaling pathway.