[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.