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- Title
2,6-Diisopropylphenol Protects Osteoblasts from Oxidative Stress-Induced Apoptosis through Suppression of Caspase-3 Activation.
- Authors
CHEN, RUEI‐MING; WU, GONG‐JHE; CHANG, HWA‐CHIA; CHEN, JUE‐TAI; CHEN, TZENG‐FU; LIN, YI‐LING; CHEN, TA‐LIANG
- Abstract
2,6-Diisopropylphenol is an intravenous anesthetic agent used for induction and maintenance of anesthesia. Since it is similar to α-tocopherol, 2,6-diisopropylphenol may have antioxidant effects. Osteoblasts play important roles in bone remodeling. In this study, we attempted to evaluate the protective effects of 2,6-diisopropylphenol on oxidative stress-induced osteoblast insults and their possible mechanisms, using neonatal rat calvarial osteoblasts as the experimental model. Clinically relevant concentrations of 2,6-diisopropylphenol (3 and 30 μM) had no effect on osteoblast viability. However, 2,6-diisopropylphenol at 300 μM time-dependently caused osteoblast death. Exposure to sodium nitroprusside (SNP), a nitric oxide donor, increased amounts of nitrite in osteoblasts. 2,6-Diisopropylphenol did not scavenge basal or SNP-releasing nitric oxide. Hydrogen peroxide (HP) enhanced levels of intracellular reactive oxygen species in osteoblasts. 2,6-Diisopropylphenol significantly reduced HP-induced oxidative stress. Exposure of osteoblasts to SNP and HP decreased cell viability time-dependently. 2,6-Diisopropylphenol protected osteoblasts from SNPand HP-induced cell damage. Analysis by a flow cytometric method revealed that SNP and HP induced osteoblast apoptosis. 2,6-Diisopropylphenol significantly blocked SNPand HP-induced osteoblast apoptosis. Administration of SNP and HP increased caspase-3 activities. However, 2,6-diisopropylphenol significantly decreased SNPand HP-enhanced caspase-3 activities. This study shows that a therapeutic concentration of 2,6-diisopropylphenol can protect osteoblasts from SNPand HP-induced cell insults, possibly via suppression of caspase-3 activities.
- Subjects
ANESTHETICS; BONE cells; OXIDATIVE stress; NITRIC oxide; APOPTOSIS
- Publication
Annals of the New York Academy of Sciences, 2005, Vol 1042, Issue 1, p448
- ISSN
0077-8923
- Publication type
Article
- DOI
10.1196/annals.1338.038