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Abstrak :
Tujuan dari penelitian ini adalah untuk menilai terjadinya aktivasi endotel sebagai mekanisme palagenesis pada preeklampsia, dengan melihat pengaruh pajanan serum penderita preeklampsia pada kultur sel endotel vena umbilikalis terhadap produksi VCAM-1. RANCANGAN PENELITIAN: Penelitian ini merupakan studi eksperimental. Kultur sel endotel yang padat (confluent) dipajankan dengan medium yang mengandung 20% serum dad wanita preeklampsia (n = 12) atau wanita hamil normal (n = 12) dengan usia, usia kehamilan dan paritas yang tidak berbeda berrnakna secara statistik. Setelah pajanan selama 24 jam, diukur kadar VCAM-1 terlarut (sVCAM-1) dalam supematan kultur sel endotel dari ke-2 populasi tersebut. Jumlah sel endotel hidup dari kultur sel endotel pasca pajanan dihitung, baik pasca pajanan serum preeklampsia maupun wanita hamil normal. Diukur juga kadar sVCAM-1 dalam medium yang mengandung 20% serum dari wanita yang sama, yang tidak dipajankan dengan preeklampsia. HASIL: Kadar sVCAM-1 dalam supematan kultur setelah pajanan pada 10.000 set endotel selama 24 jam dengan serum preeklampsia (1.366 + 0.714 ng/ml) lebih tinggi secara bermakna (P < 0.05) dibandingkan setelah pajanan dengan serum wanita hamil normal (0.735 + 0.372 nglml). Jumlah sel endotel dari kultur sel endotel setelah pajanan dengan serum preeklampsia (9.00 x 104 + 3.77 x 104) lebih rendah dibandingkan setelah pajanan dengan serum wanita hamil normal (12.67 x 104 + 6.23); tetapi perbedaannya secara statistik tidak bermakna (P > 0.05). Kadar sVCAM-1 dalam medium kuttur yang mengandung 20% serum preeklampsia yang tidak dipajankan pada kultur sel endotel (11.0516 } 5.404 ng/lml) lebih tinggi dibandingkan serum wanita hamil normal (10.417 + 6.870 ng/ml); tetapi perbedaannya secara statistik tidak bermakna (P > 0,05) KESIMPULAN: Pajanan serum penderita preeklampsia pada kultur sel endotel vena umbilicalis menyebabkan terjadinya peningkatan produksi VCAM-1 oleh sel endotel, sehingga dapat disimpulkan bahwa pads preeklampsia terjadi aktivasi endotel akibat adanya suatu zat dalam serum penderita preeklampsia. Kata kunci: Preeklampsia, aktivasi endotel, kultur set endotel vena umbilikalis, Vascular Cell Adhesion Molecule-1.

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The Effect Of Preeclamptic Sera Exposure To Human Umbilical Vein Endothelial Cell Culture To The Production Of Vascular Cell Adhesion Molecul-1 (VCAM-1) OBJECTIVE: To determine endothelial activation as a pathogenic mechanism of preeclampsia, by identifying the effect of preeclamptic sera exposure to human umbilical vein endothelial cell culture on the production of VCAM-1. STUDY DESIGN: The study was an experimental study. Confluent endothelial cell culture exposed to medium with 20 % preeclamptic sera (n=12) on women with normal pregnancy sera (n=12) with the same age, gestational age and parity. After 24-hour of exposure, cultured media were removed for measurement of VCAM-1. The concentration of sVCAM-1 in medium with 20 % sera from the same women that was not exposed to cultured endothelial cell were also measured. RESULTS : The concentration of sVCAM-1 from 10.000 cultured endothelial cells media after 24-hour exposure with preeclamptic sera (1.366 + 0.714 nglml) was significantly higher than exposure with normal pregnant women sera (0.735 + 0.372). The amount of cultured endothelial cells after exposure to preeclamptic sera (9.00 x 104 + 3.77 x 104) was lower than after exposure to normal pregnant women sera (12.67 x 104 + 6.23); but the difference was not statistically significant (P a 0.05). Without exposure to cultured endothelial cells, the concentration of sVCAM-1 in the medium with 20 % preeclamptic sera was higher (11.0516 + 5.404 nglml) than in the medium with 20% sera from normal pregnant women (10.417 + 6.870 nglml), although the difference was not statistically significant (P > 0.05). CONCLUSIONS: Exposure of human umbilical vein endothelial cell culture to preeclamptic sera increased the production of VCAM-1 by the endothelial cells. It was concluded that there was endothelial activation in preeclampsia caused by factor or factors in preeclamptic sera.

Abstrak :
Inflammatory response in the acute phase of ischemic stroke will trigger the process of neuroplasticity and determine the clinical outcomes. Angiogenesis and neurogenesis are induced by expression of vascular endothelial growth factor (VEGF) in the acute phase of stroke. The purpose of this study was to determine the association between VEGF serum level in acute of stroke with the clinical outcomes. This longitudinal cohort study was conducted on 64 patients suffering from first-attack of anterior circulation blockage as evidenced by cephalic diffusion-weighted magnetic resonance imaging (DWI). VEGF serum level was measured at 72 hours and 7 days after stroke and the clinical outcomes were assessed on day 30 post-stroke using the National Institutes of Health Stroke Scale ( NIHSS). VEGF level at hour-72 and on day-7 were 5.84+-0.736 ng/mL and 5.797 +-0.96 ng/mL, respectively (p>0.05). High VEGF levels at hour-72 can be used to predict poor clinical outcome 30 days after stroke (OR=6.5; 95% CI = 1.15-36.61 ; p=0.034). Subjects who have increasing levels of VEGF on day-7 compared to hour-72 tend to have better clinical outcomes on day-30 (NIHSS score =1.33 +-1.22 vs 3+-3.78; p=0.232). VEGF levels in the acute phase of ischemic stroke reflect the degree of brain damage, the dynamic of the increase in VEGF levels after a stroke was associated with better clinical outcomes.