The role of the endogenous anti-inflammatory compound gravidin in pre-eclampsia
Objectives: The study’s aims were to investigate the levels of gravidin, an endogenous phospholipase A 2 inhibitor, in pregnancy and pre-eclampsia and to establish its effects on neutrophil function. Study Design: Serum samples were collected from 9 nonpregnant, 15 preeclamptic, and 10 healthy pregn...
Gespeichert in:
Veröffentlicht in: | American journal of obstetrics and gynecology 1998-11, Vol.179 (5), p.1305-1311 |
---|---|
Hauptverfasser: | , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | Objectives: The study’s aims were to investigate the levels of gravidin, an endogenous phospholipase A
2 inhibitor, in pregnancy and pre-eclampsia and to establish its effects on neutrophil function.
Study Design: Serum samples were collected from 9 nonpregnant, 15 preeclamptic, and 10 healthy pregnant women and assayed for free gravidin by enzyme-linked immunosorbent assay. Neutrophil phospholipase A
2 and respiratory burst activities were determined in the presence of isolated free gravidin by cellular arachidonic acid release and superoxide anion production.
Results: Levels of free gravidin were higher in the healthy pregnant (36.1 ± 5.5 ng/mL) and preeclamptic (17.8 ± 2.8 ng/mL) groups than in the nonpregnant control group (3.9 ± 0.5 ng/mL) and were significantly different between pregnancy groups (
P < .01, Mann-Whitney
U test). Free gravidin caused a concentration dependent decrease in
N -formyl-methionyl-leucyl-phenylalanine–stimulated neutrophil arachidonic acid release (inhibitory concentration of 50% 25 nmol/L) and superoxide anion generation (inhibitory concentration of 50% 32 nmol/L).
Conclusions: Circulating levels of free gravidin are reduced in pre-eclampsia compared with normal pregnancy. This may encourage an increase in the respiratory burst of neutrophils in pre-eclampsia and could contribute to the oxidative stress and vascular damage that characterize this disease. (Am J Obstet Gynecol 1998;179:1305-11.) |
---|---|
ISSN: | 0002-9378 1097-6868 |
DOI: | 10.1016/S0002-9378(98)70152-8 |