Antioxidant Effect of Eugenol in Human Periodontal Ligament Fibroblasts
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Periodontal disease (PD) is the most common osteolytic disease of alveolar bone, oral infection seenin humans worldwide. PD is a common, chronic immunoinflammatory disease initiated by a complex subgingivalbacterial and results in the inflammatory destruction of periodontal tissues, including the alveolar boneperiodontal ligament, and gingivae. The effects of eugenol on periodontal ligament fibroblasts (PDLF) cell underoxidative injury have not been fully studied. Despite many studies in regard to the antioxidant effect of eugenol,the protective effect of eugenol against oxidative damage to PDLF cell, as well as the relationship betweeneugenol and apoptosis, has not been investigated so far. The aim of this study was to assess the protective effectof eugenol against H2O2-induced oxidative stress in PDLF cell. Cell lines were separately grown as monolayers at 5% CO2 and 37C humidified atmosphere using appropriatemedia supplemented with 10% fetal bovine serum, 2 mM glutamine and 100 μg/mL penicillin-streptomycin. DMEM/F12 was used as the culture medium for periodontal ligament fibroblast cells. The viability of the PDLF cells which induced by the different concentrations of H2O2 (control, 50, 100, 200,400 μM) for 24 h was detected by MTT assay. Cell viability was significantly reduced in a H2O2-concentrationdose-dependent manner. The mitochondria-dependent pathway of apoptosis is regulated by Bcl-xl family, such asthe anti-apoptotic protein Bcl-xl, pro-apoptotic protein Bak. With H2O2 injury, the protein level of Bak was upregulatedwhile the protein level of Bcl-xl was down-regulated. In group treated H2O2 and eugenol, the ratio wasreduced and the expression of Bak decreased at the same time, indicating that eugenol can attenuate apoptosisthrough mitochondrial related pathway in PDLF cells. Therefore, although the findings of this study are limited to an in vitro interpretation, we suggest that eugenolpreconditioning may have a beneficial effect in the recovery of periodontal ligament from oxidative stress.
Abstract
Periodontal disease (PD) is the most common osteolytic disease of alveolar bone, oral infection seenin humans worldwide. PD is a common, chronic immunoinflammatory disease initiated by a complex subgingivalbacterial and results in the inflammatory destruction of periodontal tissues, including the alveolar boneperiodontal ligament, and gingivae. The effects of eugenol on periodontal ligament fibroblasts (PDLF) cell underoxidative injury have not been fully studied. Despite many studies in regard to the antioxidant effect of eugenol,the protective effect of eugenol against oxidative damage to PDLF cell, as well as the relationship betweeneugenol and apoptosis, has not been investigated so far. The aim of this study was to assess the protective effectof eugenol against H2O2-induced oxidative stress in PDLF cell. Cell lines were separately grown as monolayers at 5% CO2 and 37C humidified atmosphere using appropriatemedia supplemented with 10% fetal bovine serum, 2 mM glutamine and 100 μg/mL penicillin-streptomycin. DMEM/F12 was used as the culture medium for periodontal ligament fibroblast cells. The viability of the PDLF cells which induced by the different concentrations of H2O2 (control, 50, 100, 200,400 μM) for 24 h was detected by MTT assay. Cell viability was significantly reduced in a H2O2-concentrationdose-dependent manner. The mitochondria-dependent pathway of apoptosis is regulated by Bcl-xl family, such asthe anti-apoptotic protein Bcl-xl, pro-apoptotic protein Bak. With H2O2 injury, the protein level of Bak was upregulatedwhile the protein level of Bcl-xl was down-regulated. In group treated H2O2 and eugenol, the ratio wasreduced and the expression of Bak decreased at the same time, indicating that eugenol can attenuate apoptosisthrough mitochondrial related pathway in PDLF cells. Therefore, although the findings of this study are limited to an in vitro interpretation, we suggest that eugenolpreconditioning may have a beneficial effect in the recovery of periodontal ligament from oxidative stress.
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