Objective: To explore the possible mechanism of mechanical factors in the pathogenesis of pelvic organ prolapse (POP).
Methods: The experiment material were uterosacral ligament and cardinal ligament- derived fibroblast from 10 patients who received total hysterectomy due to benign disease except POP. Fibroblast were cultured after collagenase digestion and identified by morphology and immocytochemical methods. Fibroblasts of 4-8 generations were stretched by four-point bending system for 0µ (0 mm), 1 333 µ (1 mm), 2 666 µ (2 mm), 5 333 µ (4 mm) strain, using 0 mm strain as the control group. Parameters was set to a frequency of 0.1 Hz, 4 hours. Cell apoptosis was tested by flow cytometry.
Results: Mechanical strain increased cell apoptosis [0 µ: (7.4 ± 1.5)%, 1 333 µ: (8.7 ± 2.2)%, 2 666 µ: (19.4 ± 3.4)%, 5333 µ: (50.9 ± 6.6)%, respectively]. Cell apoptosis rate was significantly higher under strong mechanical strain (2 666 µ and 5 333 µ versus 0 µ, all P < 0.05).
Conclusion: Increased mechanical stress loading on human parametrial ligament fibroblasts could raise the rate of apoptosis.