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Background and Aim: Endometriosis affects the ovaries and causes a decrease in the oocyte quality during endometrial receptivity. During the development of ovarian follicles, paracrine communication occurs between granulosa cells and oocytes. This study was conducted to determine the effects of bone marrow mesenchymal stem cell transplantation on tumor necrosis factor-alpha (TNF-α) receptor 1 (TNFR1) expression, granulosa cell apoptosis, and folliculogenesis in endometriosis mouse models. Materials and Methods: This study involved 42 female mice, which were divided into three groups: Healthy mice (T0), endometriosis mice without transplantation (T1), and endometriosis mice with bone marrow mesenchymal stem cell transplantation (T2). The mice were injected intraperitoneally with endometrial fragments (200 μL) to become endometriosis models. On day 15, the endometriosis models received mesenchymal stem cells. Sample collection was performed on day 29. Granulosa cell apoptosis and TNFR1 expression were examined using immunohistochemical staining, and folliculogenesis was assessed using hematoxylin and eosin staining of ovary samples. The data obtained from both examinations were statistically analyzed using Statistical Package for the Social Sciences. Results: The results showed that TNFR1 expression is significantly decreased in T2 (p<0.004). The apoptosis of granulosa cells was lower in T2 (p<0.000). The primary, secondary, and graafian follicle counts in T2 were significantly increased. Conclusion: Bone marrow mesenchymal stem cell transplantation in endometriosis mouse models can reduce TNFR1 expression and granulosa cell apoptosis and improve folliculogenesis.

A study was designed to investigate ameliorates effect of combined vitamins C and E able to against depot-medroxyprogesterone acetate- (DMPA-) induced ovarian oxidative stress in rat. Twenty-five female Wistar rats were divided into the following groups (n = 5 rats each): control (untreated) (C); depot-medroxyprogesterone acetate (DMPA); DMPA plus green vitamin C (at dose of 0.2 mg/gram; 0.4 mg/gram; 0.8 mg/gram) and vitamin E (0.04 IU/gram). The treatment with combined vitamins C and E was performed for four weeks. Analysis of malondialdehyde (MDA) level as a marker of oxidative stress was done colorimetrically. Analysis of SOD level was done by enzyme linked immunosorbent assay (ELISA) technically. This increase in ovarium MDA was significantly (P < 0.05) attenuated by medium dose treatments of combined vitamins C and E. DMPA insignificantly decreased SOD levels compared to the untreated group. This decrease in ovarian SOD level was significantly attenuated by all doses of the combined vitamins C and E. In conclusion, DMPA induces ovarian oxidative stress. Combined vitamins C and E prohibit the increase in ovarian lipid peroxidation, at least in part by modulating of superoxide dismutase. Therefore, this may provide an antioxidant therapy for attenuating the ovarian toxicity found in the DMPA therapy.

Background: Indonesian seawater has been found to contain a high level of lead acetate and tends to become toxic. The previous study suggested lead acetate exposure could be harmful to many organs including the brain, liver, heart, as well as the reproductive system. This study aimed to analyze the effect of lead acetate on both the uterine level of malondialdehyde (MDA) level and endometrial thickness in female Wistar rats (Rattus norvegicus).Methods: Twenty-four rats were divided into 4 groups: 1 control group, and 3 treatment groups that were given lead acetate at 30, 100, and 300 ppm p.o./day for 30 days, consecutively. Rats were sacrificed; the uterus was isolated and processed for both MDA level measurements (using TBARS and a spectrophotometer) and histopathology using hematoxylin-eosin (HE) staining. Results:There was no significant difference in mean MDA level between the control and lead acetate administration groups. There was a reduction in endometrial thickness from 352.6±81.88 µm in the control group to 323.5±90.67 µm; 313.6±40.30 µm; 303.4±62.75 µm in 30, 100, and 300 ppm, respectively. Consequently, spacious uterus was observed reflects the endometrial damage, including the decrease in the size of the epithelium, columnar, stroma, and lumen in the whole part of the uterus and these differences in uterine thickening was considered statistically significant (p=0.005). Conclusion:Lead acetate could reduce the thickness of the endometrium but had no effect on the level of MDA in the uterus.

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Background: Endometriosis and infertility are caused by reactive oxygen species or free radicals, which promote endometrial cell growth and adhesion in the peritoneal cavity. Genistein has been proven to protect cells against reactive oxygen species by scavenging free radicals and decreasing the expression of genes-associated stress responses. Objective: This study was conducted to determine whether genistein also acts as an antioxidant by elevating superoxide dismutase (SOD) and glutathione peroxidase (GPx) in the peritoneal fluid of the endometriosis mice model. Materials and Methods: This experimental study involved 32 healthy female mice (Mus musculus), aged between 2-3 months and weighing 20-30 gr. They were divided into negative control group (healthy mice without genistein), endometriosis group (endometriosis mice without genistein), treatment group that was given different doses of genistein, that is, 0.13; 0.26; 0.52; 0.78; 1.04; and 1.3 mg/day (n = 4/each). SOD level in the peritoneal fluid was measured using the quantitative colorimetric determination method, and a colorimetric assay measured the GPx levels. Results: Results showed that the endometriosis model has lower SOD and GPx levels than the control group. The administration of genistein significantly normalized these changes. Genistein significantly increased SOD levels in the 0.13 mg and 0.26 mg treatment groups. Genistein also increased GPx levels significantly in all treatment groups. Conclusion: Genistein increases SOD and GPx levels in the peritoneal fluid of an endometriosis mice model, and the change is dose-dependent. Key words: Superoxide dismutase, Glutathione peroxidase, Endometriosis, Genistein.

Background: Measles vaccinations have been suggested to provide immune protection and decreased measles incidence. However, there was a limited study evaluating how the measles vaccine elicits specific immune responses.Objective: This study aimed to evaluate both humoral and cellular immunity to first-dose measles vaccine Edmonston-Zagreb (EZ) in 9-month-old Indonesian infants.Methods: A cohort study was conducted on 9-month-old infants who got the first-dose of measles vaccine EZ. Measles-specific immunoglobulin G (IgG) antibody serum levels were measured using plaque-reduction microneutralization assay. Peripheral blood mononuclear cells were stimulated with a measles-specific peptide to identify a cellular immune response. Quantification of CD4+ and CD8+ T-cells producing interferon-gamma (IFN-ɣ) and interleu-kin 17-A (IL-17A) were conducted by flow cytometry. Humoral and cellular immune response parameters were analyzed over time.Results: The prevalence of seropositivity rates was 85.8% at 1-month after vaccination and 16.67% at 6-months postvaccination. Measles-specific IgG antibodies increased significantly at 1-month after measles vaccination. However, they decreased significantly 6-months after vaccination. IFN-ɣ and IL-17A secreting T-cells increased significantly at 1-month after measles vaccination. Interestingly, a significant decrease of IFN-ɣ and IL-17A secreting CD4+ T cells was noticed 6-months postvaccination compared to IFN-ɣ and IL-17A secreting CD8+ T cells. Conclusion: Our study suggests that the first-dose measles vaccine on 9-months-old infants seems to induce both humoral and cellular immune responses that decline 6-months after vaccination.