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Background and Aims: Previous studies have explored the role of neurotrophins and their receptors, especially in forming deep endometriosis, endometriosis tissue invasion, and its effects on tissue proliferation. However, these studies do not include research on the pathogenesis of endometriomas. We tried to model the invasion of endometrioma tissue to find out more about its pathogenesis by using the chorioallantoic membrane (CAM) as the host. Immunohistochemistry (IHC) to detect neurotrophin BDNF and its receptors, namely TrkB and P75, are employed and linked between their expression and the process of invasion and proliferation.Method: The endometriotic tissue samples were collected from women (n=27) who underwent hysteroscopy/laparoscopy at Dr. Sardjito Central Hospital. Peritoneal endometriosis (PE) lession, endometrioma (CC), and eutopic endometrium (EN) was analyzed with 15 tissue samples in each group. Samples were placed in a tube containing transport medium and transplanted into CAM of fertile chicken eggs for five days. Transplanted tissue was harvested, and histological preparations were made using the paraffin method. IHC staining was performed on p75, Ki67, TrkB, and BDNF staining. Invasion analysis and IHC evaluation were performed with a semi-quantitative method. Data were analyzed using IBMⓇSPSS Statistics version 25.0. Statistical significance was accepted at P < 0.05.Results: Normal Endometrium expressed the highest expression of BDNF than peritoneal endometriosis and endometrioma (0.36± 0.38, 0.16± 0.13, 0.07± 0.07, P=0.007). The P75 expression correlated positively with Ki67 expression in PE and CC samples (P=0.012; P=0.008).Conclusion: The p75 receptor may have a role in endometriosis tissue proliferation, but this receptor does not directly influence tissue invasion into CAM. While proliferation in endometriomas positively correlates with invasion into CAM, it is not correlated with peritoneal endometriosis.

Background and Aims: Several studies have found that diet is critical during a female’s pregnancy. The nutritional condition of pregnant women can have long-term consequences for their children, particularly the growth of the reproductive system. However, previous studies have various opinions regarding whether or not the nutritional status of the maternal correlates with seminiferous tubule diameter and the Sertoli cell amount of their offspring. This study aims to observe the effect of low protein diet on pregnant mice towards the offspring’s seminiferous tubule diameter, Sertoli cell, and vacuole.Method: Ten female ddY mice were split into two groups and given two months of treatment with either a normal protein diet (14%) or a low protein diet (10%). The mice were mated to produce offspring after treatment. Each group had five male progenies that were raised until they were three months old before being terminated to retrieve their testicles. Hematoxylin-eosin staining was used for histological analysis of the testicle sample. Testicles samples were observed for seminiferous tubule, Sertoli cell, and vacuole. Data was presented as mean & standard deviation. ANOVA and the Mann-Whitney U test was used to analyze the data. Statistical significance was accepted at p<0.05.Results: There were no statistical differences between the offspring’s seminiferous tubule diameter and Sertoli cell count in the normal protein diet group and the low protein diet group (6.28±1.79 vs 6.47±0.79; 4.72±3.13 vs 4.84±2.81). On the contrary, the low protein diet group has a higher vacuole amount than the normal protein diet group (6.76±4.59 vs 3.64±3.07; P=0.004).Conclusion: A maternal low-protein diet did not affect the Sertoli cell population or the length of the child’s seminiferous tubules but led to a significant increase in vacuoles.