[Mechanism of advanced glycation end-products in the inducement of apoptosis of human gingival fibroblast and related effect of puerarin in the process].

Objective: To observe the effect of synthesized advanced glycation end-products (AGE) on reactive oxygen species formation and apoptosis of the cultured human gingival fibroblast and investigate the potential mechanisms of AGE in the modification of periodontal impairment.

Methods: AGE products with different concentrations [0, 50, 150 mg/L AGE-human serum albumin (AGE-HSA)] were incubated with human gingival fibroblast for 48 h, respestively. Flow cytometry was used to detect intracellular reactive oxygen species and cell apoptosis. The culture media with 50 mg/L AGE-HSA was exposed to 0.24 mmol/L puerarin for 48 h and then cell apoptosis was measured.

Results: The values of cellular apoptotic rate in 0, 50, 150 mg/L AGE-HSA groups were (1.60 ± 0.30)%, (29.43 ± 1.45)%, (49.20 ± 4.43)%, respectively. The differences between each AGE-HSA group and control were statistically significant (P < 0.05). AGE-HSA increased cell apoptosis in a dose-dependent manner (150 mg/L > 50 mg/L > 0 mg/L, P < 0.05). The cellular fluorescence intensity value was elevated as the concentration of AGE-HSA increased (P < 0.05). After incubation of human gingival fibroblast with AGE-HSA for 48 h, there was a significant decrease in apoptotic rate in puerarin group [(6.37 ± 3.02)%], compared with the control [(29.43 ± 1.45)%, P < 0.05].

Conclusions: AGE can stimulate apoptosis of human gingival fibroblast, which may be mediated by oxidative stress. Puerarin may protect periodontal tissues by inhibiting the apoptosis.