Loeki E Fitri, Loeki E
PARASITOLOGI FK UNIVERSITAS BRAWIJAYA MALANG

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Injeksi Serum Mengandung TNF-α Tinggi Menurunkan Konsentrasi VEGF dan Ekspresi Nephrin Glomerulus Mencit Bunting Agmar, Syahroni Yudistian; Windu Batiyani, Siti Candra; Fitri, Loeki E
Jurnal Kedokteran Brawijaya Vol 29, No 1 (2016)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jkb.2016.029.01.3

Abstract

Preeklampsia ditandai dengan adanya hipertensi dan proteinuria pada usia kehamilan lebih dari 20 minggu. Preeklampsia diderita oleh 3%-8% wanita hamil dan menjadi penyebab utama kematian pada kehamilan. Tumor Necrosis Factor-α(TNF-α) diduga memiliki peranan penting dalam menimbulkan terjadinya preeklampsia. Tujuan dari penelitian ini adalah untuk mengetahui efek injeksi serum dengan konsentrasi TNF-α tinggi terhadap konsentrasi Vascular Endothelial Growth Factor (VEGF) dan ekspresi protein nephrin glomerulus  pada mencit bunting. Serum dengan konsentrasi TNF-α tinggi diambil dari ibu hamil dan diinjeksikan intraperitoneal pada mencit bunting dengan usia kebuntingan 13 dan 14 hari. Pada usia kebuntingan 18 hari konsentrasi VEGF serum diperiksa menggunakan ELISA dan ekspresi protein nephrin glomerulus dengan imunohistokimia. Penelitian ini menunjukkan injeksi serum TNF-α dapat menurunkan konsentrasi VEGF serum mencit bunting (p=0,021) dan ekspresi protein nephrin glomerulus (p=0,000). Penurunan konsentrasi VEGF dan protein nephrin terjadi pada pasien preeklampsia dan dapat menimbulkan gejala preeklampsia. Dapat disimpulkan bahwa injeksi intraperitoneal serum dengan konsentrasi TNF-α tinggi dapat memberikan gambaran preeklampsia pada mencit bunting. 
Haemozoin Deposits Influence Fetal Weight of Pregnant Mice Infected by Plasmodium berghei Andari, Desy; Fitri, Loeki E; Mintaroem, Karyono
Jurnal Kedokteran Brawijaya Vol 28, No 4 (2015)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (836.275 KB) | DOI: 10.21776/ub.jkb.2015.028.04.4

Abstract

Low birth weight is commonly attributed to malaria in pregnancy, but the cellular and molecular mechanisms that underlie this are incompletely understood. Many of hormones and cytokines are dysregulated in this case and it alters histological structure of placenta which known as placenta malaria. In the placenta malaria, there is an accumulation of infected erythrocytes, macrophages and malarial pigment (haemozoin). This study was conducted to compare the levels of plasma and placenta interferon-gamma (IFN-γ) and haemozoin deposit in pregnant mice that infected by Plasmodium berghei (treatment group) to the normal pregnant mice (control group) and its association with fetal weight. This in vivo experimental laboratory study used pregnant Balb/c mice which divided to control and treatment group. Placentas were staining with Haematoxylin-Eosin (HE) for haemozoin deposits examination. Plasma and placenta levels of IFN-γ examined with ELISA assay. Levels of IFN-γ were higher in plasma than placenta and slightly higher in treatment group than control group, but the differences were not significant (p>0,05). Fetal weight of treatment group was lower than those of control group (p=0,002) however there was no correlation between fetal weight and plasma as well as placenta levels of IFN-γ (p>0,05). Haemozoin deposit was found only in treatment group and influenced weight of fetuses (Spearman=-0,633, p=0,006). Weights of fetuses are more interfered by haemozoin deposit and seemly not by plasma and placenta levels of IFN-γ during malaria infection.Keywords: Fetal weight, gamma interferon, haemozoin, malaria, placenta
High Level of Plasma Tumour Necrosis Factor-α (TNF- α) in Pregnant Mice Infected with Plasmodium berghei is Strongly Related to Low Level of Hemoglobin but not Related to Fetal Low Weight Yuliyanik, Yuliyanik; Fitri, Loeki E; Sardjono, Teguh Wahju
Jurnal Kedokteran Brawijaya Vol 28, No 4 (2015)
Publisher : Fakultas Kedokteran Universitas Brawijaya

Show Abstract | Download Original | Original Source | Check in Google Scholar | DOI: 10.21776/ub.jkb.2015.028.04.3

Abstract

Malaria infection in pregnancy may increase the morbidity and mortality for both mother and fetus. In pregnant women, it can lead to severe anemia, cerebral malaria, pulmonary edema, renal failure and even death, while in the fetus it can cause abortion, premature birth, low birth weight, and fetal death. Elevated levels of tumor necrosis factor-α (TNF-α ) are associated with low birth weight and anemia in pregnant women. This study was conducted to measure the levels of TNF-α in plasma and hemoglobin levels as well as fetal weight to determine the relationship among them in P. berghei infected pregnant mice and normal pregnant mice. Seventeen BALB/c mice used in this study were divided into two groups, those were the study group (9 pregnant mice infected with P. berghei) and control group (8 pregnant mice not infected with P. berghei). Levels of TNF-α were measured using Enzyme Linked Immunosorbent assay (R&D Systems, catalog A00B MT). Hemoglobin levels were determined using flowcytometri, whereas fetal weights were measured with Mettler analytical balance AE 50. T-test statistical analysis showed that the levels of plasma TNF-α in study group were higher than control group (p=0,000). Hemoglobin levels in the study group  were lower than control group (p=0,025). Fetal weights were also lower in fetuses of infected mice than fetuses of uninfected mice (p=0,002). Pearson correlation test showed that increasing plasma levels of TNF-α in infected P. berghei pregnant mice were related with the decreasing levels of Hb, (p=0,020; r=-0,748).  However plasma levels of TNF-α were not associated with the incidence of fetal low weight (p=0,380, and p=0,365). It can be concluded that the increasing levels of TNF-α is associated with decreasing levels of hemoglobin (Hb), but not associated with fetal low weight.Keywords:  Birth weight, hemoglobin, Plasmodium berghei, Tumour Necrosis Factor-α (TNF- α)