Objective To establish a rat animal model that can reflect the similar pathological changes of the sacral ligament in patients with pelvic organ prolapse, to explore the effects of increasing the intensity of birth trauma and simulating menopause on the histopathology of the sacral ligament in rats, and to provide an experimental basis for further research.
Methods Sixty adult SPF female SD rats weighing about 300 g were selected, of which 45 had no reproductive history, and were randomly divided into blank control group (A), simulated menopause group (B), simulated birth trauma + The simulated menopause group (C), and the other 15 who had three consecutive deliveries were the birth trauma + simulated birth trauma + simulated menopause group (D). Group A was given normal drinking and eating, group B was given double oophorectomy, group C was given simulated birth trauma operation and bilateral oophorectomy to simulate menopause, and group D was given two simulated birth trauma on the basis of three consecutive deliveries Ovariectomy was performed to simulate menopause, and they were routinely fed for 8 to 10 weeks after surgery. Eight rats were randomly selected from each group, and the appearance of the genitals and the changes of genital tract holes were observed; immunohistochemical method was used to observe and evaluate the type I and III collagen (COL1A1, COL3A1), transforming growth factor β-3 ( TGFβ-3) integrated optical density changes. The mRNA expression levels of COL1A1, COL3A1 and TGFβ-3 in sacral ligament tissue were determined by RT-PCR.
Results After modeling, the diameter of the vaginal hiatus of the rats in group D was greater than that of the control group by more than 2 mm. There was no obvious prolapse phenotype in the rats in each group, and group D showed mild abnormality of the perineal body; The expression of COL1A1 was significantly lower than that in group A (P<0.05), and the relative expression of TGFβ-3 in group C and D was significantly higher than that in group A (P<0.05); The expressions of COLIA1 and COL3A1 in the ligaments were significantly lower than those in group A (P<0.05), and the relative expression of TGFβ-3 in groups C and D were significantly higher than those in group A (P<0.05).
Conclusion The genital prolapse phenotype of the rat model after modeling is not significant. For example, it is not suitable to study the phenotypic changes. This model can be used as an animal model to study the pathophysiological changes of POP sacral ligament. However, it is uncertain whether the mechanical properties of human and rat sacral ligaments are similar, and the most suitable animal model should be selected based on the advantages and disadvantages of various animals and the practical research problems to be solved.