Wiyasa, I W.A.
Division of Fertility, Endocrinology and Reproduction, Obstetric and Gynaecology Laboratory, Saiful Anwar Hospital, Faculty of Medicine, Universitas Brawijaya, Malang

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The effect of lead acetate administration to the uterine malondialdehyde level and endometrial thickness in albino rats (Rattus novergicus) Diantini, Novita S.E.; Soeharto, Setyawati; Wiyasa, I W.A.
Medical Journal of Indonesia Vol 27, No 3 (2018): September
Publisher : Faculty of Medicine Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (858.073 KB) | DOI: 10.13181/mji.v27i3.2031

Abstract

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.
Curcumin induces apoptosis in trophoblast model cell line Nurseta, Tatit; Irwanto, Yahya; Wiyasa, I W.A.; Rahajeng, Rahajeng; Imelda, Imelda; Ratnawati, Putu A.R.
Medical Journal of Indonesia Vol 27, No 2 (2018): June
Publisher : Faculty of Medicine Universitas Indonesia

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (662.616 KB) | DOI: 10.13181/mji.v27i2.1821

Abstract

Background: Several studies have reported that curcumin exerts chemopreventive effects in various type of cancers, through several mechanisms, however, the effect of curcumin on carcinogenesis in patients with hydatidiform mole has not yet been investigated. This study was conducted to evaluate the effect of curcumin on apoptosis, proliferation, and nuclear translocation of endothelial nitricoxide synthase in trophoblast cells induced by estradiol in complete hydatidiform mole (CHM).Methods: In this in vitro study, trophoblast cells were divided into six groups, the control group (trophoblast cells were exposed to 100 pg/mL of 17-β estradiol) and the treatment group (trophoblast cells were exposed to 100 pg/mL of 17-β estradiol in the presence of curcumin with doses: 50, 100, 200, 400, and 800 µM). At the end of study, the cell proliferation was analyzed using MTT assay and apoptosis with TUNEL test in each group thropoblast cell. eNOS translocation was assayed using confocal laser scanning microscopy at the various dose of curcumin.Results: Curcumin at the doses of 200, 400, and 800 µM significantly decreased the proliferation and increased the apoptotic index in curcumin-treated group compared to those in the control group (p<0.05). All doses of curcumin treatment significantly decreased the nuclear eNOS expression compared to that in the control group. The three highest doses of curcumin increased cytoplasmic eNOS expression compared to that in control group.Conclusion: Curcumin inhibits the proliferation and modulates the apoptosis of trophoblast cells induced by estradiol in CHM involvement.