Abstract
We have previously demonstrated that gingival fibroblast obtained from nifedipine reactive patients (nifedipine responder, NIFr) was found to possess higher proliferative activity than fibroblasts obtained from nifedipine non-reactive patients (nifedipine non-responder, NIFn) or normal gingival fibroblast (nifedipine non-treated gingival fibroblast) . 18α-Glycyrrhetinic acid (18α-GA), a constituent of licorice, is a good anti-proliferative agent especially on those cells whose replication rate is slow, by inhibiting the onset of progression. Thus, we examined the effect of 18α-GA to clarify whether it depresses the growth of NIFr. 18α-GA inhibited cell proliferation and G1/S transition induced by bFGF in NIFr cells. It was also shown that cell cycle control proteins, such as pRB (ser780), pRB (ser807/811), CDK4, CDK6, CDK2, cyclin D1, and cyclin A, were down-stream targets in the growth-inhibition activity of 18α-GA in NIFr cells. In the development of nifedipine-induced gingival overgrowth, an inflammation and the cell growth of NIFr cells are important factors. Based on these findings, 18α-GA, which has anti-inflammatory effect and inhibits growth of NIFr cells, may have a positive role in nifedipine-induced gingival overgrowth therapy.
