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INTRODUCTIONPrematurity causes neonatal mortality and morbidity. Nearly half of neonatus who are survive will have congenital neurological disability including cerebral palsy (CP). The incidence of CP and cognitive impairment associated with periventricular white matter damage, which is often found in infants who are born before pregnancy of 32 weeks or acquired corticosubcortical abnormalities in term newborns (Degos V et al .2008). Pro-inflammatory cytokines is known significantly increased in the amniotic fluid and fetal brain of neonatus with infection, including local inflammatory response that causes damage to the fetal brain. Microbial infections in the amniotic fluid can cause premature labor and result to a fetal infection. Microorganisms produce a product that can trigger mononuclear cells to produce IL-1 and TNF-, which can increase the permeability of the blood brain barrier so that the products of microorganisms and pro-inflammatory cytokines that can enter the brain and cause tissue damage to the brain's white matter (white matter damage) of fetus. The latest hypothesis states that the cause of pre-eclampsia is more in focus to the immune response. Cytokines are regulator of immune substances that involved in the pathogenesis of pre-eclampsia. Successful pregnancy is a Th2 phenomenon, in which the Th1 / Th2 shift to a Th2-type response. Type 1 cytokines including interleukin-2, interferon (IFN) and tumor necrosis factor alpha (TNF-) are occured in pre-eclampsia caused by inflammation (Mirahmadian et al, 2008). Plasma concentration of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-) and interleukin 1 (IL-1) in patients with pre-eclampsia compared to normal pregnant women.Cytokine TNF- is a 17kd peptide, which is a soluble mediator of cellular immunity. (Gulti et al, 2005). Some researchers have demonstrated that TNF levels serum are significantly higher in first trimester and second trimester among pregnant women who developed into pre-eclampsia compared to the group of control. Based on research conducted by Kocyigit et al, concentration of TNF- is higher in pre-eclampsia. (Kocyigit et al, 2004). Some studies suggested that infections and inflammatory processes are associated with pre-eclampsia. IL-1 secretion initiated pro-inflammatory cascade, including the production of TNF-, interferon gamma (IFN-), IL-2, and IL-12. IL-1 gene family located on chromosome 2q13-14. IL-1 gene is the most high polymorphic and several polymorphisms diallelic have also been researched. In pre-eclampsia, pro-inflammatory cytokine IL-1 and TNF- as the mediator of inflammatory response by attracting and activating leukocytes in tissues and stimulates the secretion of lymphocytes cytokines and catabolic enzymes which involved in oxidative stress associated with pre-eclampsia. Mechanisms of inflammation and infection in the pathogenesis of pre-eclampsia is very significant in developing countries, where the highest incidence of subclinical chronic infections may be one cause of the high incidence of pre-eclampsia. (Tavakol et al, 2005).Pathologic lesion that is most common associated with Cerebral Palsy (CP) in premature infants is Periventricular White Matter Injury (PWMI). Oligodendrocyte gather most in White Matter glia in the brain. N-methyl-D-aspartic acid (NMDA) receptors on oligodendrocyte is very important in the process of damage to the Glia. Antagonist receptor of N-methyl-D-aspartic acid (NMDA) become potential neuroprotective agent in some animal models of brain damage in pregnancy. Mediator of inflammation cause damage to the developing brain by different way, as TNF-1, plays an important role in the immune process which causes damage to periventricular White Matter in fetus/ neonatus. Cytotoxic and inflammation processes of TNF- occurs through the membrane among the TNF-R1 receptors. TNF-R1 has intracellular areas which have been dead and the activation regulates cell apoptosis. Aberrant signal of TNF-/ TNF-R1 has a potential rule in the early pathogenesis of brain damage, in which oligodendrocytes that have been dead and demyelination is the primary pathology factor in this process. TNF-R1 expression in oligodendrocytes significantly increased in Perivetrikular White Matter of the brain that is growing. It is paired with the increase of death cell caused by apoptosis and necrosis in the Periventricular White Matter. So it appears that the production of TNF- by microglial cells in hypoxic conditions induces apoptosis of oligodendrocytes through TNF-R1. Unlike TNF-, IL-1 is not toxic to the oligodendrocytes, but it can block the proliferation of oligodendrocytes. This has been researched about the significant increase in production of IL-1 by microglial cells coincide with the expression of IL-1 receptor in oligodendrocytes in the periventricular white matter of neonatal brain. It is estimated that the activation and orientation of pro-inflammatory of the production of IL-1 by microglial cells in hypoxic conditions inhibit the development of white matter and the improvement of the hypoxic condition. (Berger et al 2012).In human, magnesium is very important in cellular processes, including glycolysis, oxidative phosphorylase, synthesis of proteins, DNA and RNA aggregation and maintain the plasma membrane. Magnesium has a beneficial effect on cell death by reducing cytokine pro-inflammation or free radicals formed during the process of hypoxic-ischemia reperfusion and inflammatory processes in pregnancy. Magnesium keep excitotoxic calcium which causes tissue damage, by non competative voltage-dependent inhibition of N-methyl-D-aspartate (NMDA) glutamate receptors to reduce the influx of calcium into the cell. Infant and fetal brains are more susceptible to damage by glutamate. Agents block the glutamate receptors such as magnesium sulfate may reduce the risk of tissue damage in the perinatal period. Magnesium has a beneficial hemodynamic effects including stabilize the blood pressure during the first two days in the life of preterm fetus and can increase cerebral blood flow by reducing constriction of the cerebral arteries. Transfer of transplacental magnesium can happen quickly, will increase the concentration of magnesium in the blood serum of fetal just within an hour after administration of magnesium to the mother. (Crowther et al .2013)In another study showed that levels of intracellular magnesium increased when given MgSO4 therapy. MgSO4 will pass through the placenta so that its concentration in maternal and fetal become equivalent. Its anti-inflammatory effects are reversible, magnesium will reduce cytokine production and is not associated with the changes of osmotic pressure. MgSO4 also decrease cytokine and gene expression IB. In addition, it also reduces the phosphorylation level of NF-B P56 and NF-B nuclear location following the TLR4 stimulation. And reduce the production of cytokines will cancel the function of NF-B inhibitors, this proves that MgSO4 affects cytokine production in NF-B dependent behavior. MgSO4 reduce the presentation of monocyte TNF production and IL-6 following the TLR2 / 6 agonist exposure. Magnesium suplement increases the level of IB, thus reducing NF-B activation and cytokine production. (Sugimoto et al, .2012)

MATERIALS AND METHODSThis research is an analytic research using cross sectional with clinical trials approach the levels of TNF and IL-1 in preterm pregnant women using MgSO4 and without MgSO4 by using ELISA method.This study was conducted on 40 pretem pregnant women, a single fetus with good nutritional status who delivered in Dr. Moewardi Surakarta hospital were divided into 2 groups: 20 pretem pregnant women were given MgSO4 and 20 pretem pregnant women were not given MgSO4, which all these samples are qualified with the inclusion and exclusion criterias.Blood sampling performed in the umbilical vein 10 ml, then each of it 5 ml for examination of serum IL-1 and TNF-. Given lable to the blood sample tube, name and register, then centrifuge at a speed of 2000-3000 rpm for 15 minutes, then serum was stored in a refrigerator at a temperature of -20 C and later sent to Jakarta using ice packs and being worked in the PRODIA Laboratory at Jakarta. The examination of serum level of IL-1 and TNF- is done by using the quantitative ELISA method.Data obtained from the serum levels of TNF and IL-1 in premature pregnancy who are given MgSO4 and who are not given MgSO4 were collected and statistically compared using the t test by using SPSS for windows version 17:00.

RESULTSFrom the data obtained that the average maternal age variable is 4:20 24.82 + years with the mean of gestational age 33.52 + 1:50 weeks, the mean of hemoglobin levels 10.61 + 1:09 gr / dl, the mean of albumin levels 1,361.16 12,682.50 + (103 / ml), random blood sugar 103.40 + 13:17 (mg / dL), the mean of AST 8:09 28.27 + U / I, SGPT with mean 26.60 + 7:59 U / I, the mean of TNF-alpha 2:52 + 0.76 ng / mL and the mean of IL-1 beta 0.60 + 0:27 ng / mL.Statistical analysis using the Kolmogorov-Smirnov normality test for research variable of maternal age, gestational age, hemoglobin, albumin, random blood sugar, SGOT and SGPT in preterm pregnant group given MgSO4 and preterm pregnant group without given MgSO4 do not have significant differences/ homogeneous (Kolmogorov-Smirnov> 0.05). Table 1.From the results of mean difference test of preterm pregnant given MgSO4 group and preterm pregnant group without given MgSO4, it is found that maternal age, gestational age, albumin, number of platelets, random blood sugar and SGPT are significantly different in statistis (p 0.05). Table 2.

Normality Test of TNF-alpha and IL-1 betaVariable analysis of TNF- and IL-1 by using normality test (Kolmogorov-Smirnov) in group of preterm pregnant women given MgSO4 and group of preterm pregnant women without MgSO4 normally distributed with TNF- p value = 0.71 (p> 0.05) and IL-1 p = 0.95 (p> 0.05) for group of pregnant women given MgSO4. TNF- p = 0:39 (p> 0.05) and IL-1 p = 0.76 (p> 0.05) for preterm pregnant women group who were not given MgSO4, so TNF-alpha and IL-1 in the group of preterm pregnant women given MgSO4 and preterm pregnant women group without given MgSO4 are homogeneous.Results of the mean distribution of TNF-alpha appears lower in the group of preterm pregnant women given MgSO4 (2:24 + 0:56 ng / mL), compared to preterm pregnant group without given MgSO4 (2.80 + 0.85 ng / mL). The interpretation of the graph shows that the decreased levels of TNF-alpha in preterm pregnant group given MgSO4 having a lower peak than the levels of TNF-alpha in preterm pregnant group without given MgSO4. (Figure 1.) Table 3T test analysis using = 0:05 proves that TNF-alpha levels between preterm pregnant group without given MgSO4 and preterm pregnant group given MgSO4 have there are significant differences with p = 0:01 (