IADR Abstract Archives
Enoxolone (18β-glycyrrhetinic acid) in gingival inflammation management : an in vitro study
Objectives: Arthrodont® range is a product line of oral healthcare, primarily indicated for gum inflammation treatment. One of the active ingredients is enoxolone (18β-glycyrrhetinic acid) which is recognized as a Nonsteroidal anti-inflammatory drug. An in vitro inflammatory gingival model has been designed to study its pharmacological activity. In particular, we have investigated its ability to modulate inflammatory cytokines expressed by gingival keratinocytes and known to be involved in gingival inflammatory disease..
Methods: Primary gingival keratinocytes were established from gingival human tissue samples. Cells were either stimulated or not with mediators of inflammation like TNFα and IL1β and were incubated with assay medium containing the test compound (enoxolone) or the positive control compound (dexamethasone). IL1α, IL6 and IL8 productions in cell culture supernatants were measured by ELISA. Gene expression of inflammatory actors was assessed by real-time polymerase chain reaction.
Results: When using this in vitro model, we have shown that firstly, the gingival model was able to respond to TNFα + IL1β mix by producing and secreting IL1α, IL6 and IL8. The presence of dexamethasone led to a significant inhibition of inflammatory response. Secondly we have shown that in the presence of enoxolone, the keratinocyte inflammatory response was also significantly reduced too. The decrease of pro-inflammatory cytokines production was the same as with dexamethasone. Third, the treatment of gingival keratinocytes with enoxolone did not lead to a complete extinction of inflammatory response.
Conclusions: Together this data demonstrated that the use of enoxolone modulates an inflammatory gingival response. Indeed, it allows for a significant reduction of the expression of cytokines largely involved in inflammatory gingival disease. Our data suggest that 18β-glycyrrhetinic acid may provide a modulation of gingival inflammatory response, through attenuating IL1α, IL6 and IL8 secretion. Therefore, these in vitro results confirm the action of enoxolone in the gingival inflammation process.
Methods: Primary gingival keratinocytes were established from gingival human tissue samples. Cells were either stimulated or not with mediators of inflammation like TNFα and IL1β and were incubated with assay medium containing the test compound (enoxolone) or the positive control compound (dexamethasone). IL1α, IL6 and IL8 productions in cell culture supernatants were measured by ELISA. Gene expression of inflammatory actors was assessed by real-time polymerase chain reaction.
Results: When using this in vitro model, we have shown that firstly, the gingival model was able to respond to TNFα + IL1β mix by producing and secreting IL1α, IL6 and IL8. The presence of dexamethasone led to a significant inhibition of inflammatory response. Secondly we have shown that in the presence of enoxolone, the keratinocyte inflammatory response was also significantly reduced too. The decrease of pro-inflammatory cytokines production was the same as with dexamethasone. Third, the treatment of gingival keratinocytes with enoxolone did not lead to a complete extinction of inflammatory response.
Conclusions: Together this data demonstrated that the use of enoxolone modulates an inflammatory gingival response. Indeed, it allows for a significant reduction of the expression of cytokines largely involved in inflammatory gingival disease. Our data suggest that 18β-glycyrrhetinic acid may provide a modulation of gingival inflammatory response, through attenuating IL1α, IL6 and IL8 secretion. Therefore, these in vitro results confirm the action of enoxolone in the gingival inflammation process.