Abstract

To research the correlation of the expressions of lipocalin-2 (LCN-2) and its receptor (NGALR) in serum and placenta with preeclampsia. From Dec.2010 to Apr.2011, 64 women with preeclampsia who delivered in Affiliated Hospital of Qingdao University Medical College were recruited in the study, including 26 women with moderate preeclampsia (MPE group) and 38 women with severe preeclampsia (SPE group). Twenty-five healthy pregnant women were taken as control group. LCN-2 and NGALR mRNA and protein expression in placenta were measured by reverse transcription-PCR (RT-PCR) and western blot, respectively. (1) The serum levels of LCN-2 in MPE group and SPE group [(58 ± 20), (90 ± 18) µg/L] were significantly higher than that in control group [(19 ± 6) µg/L, P < 0.01]; the serum LCN-2 level in SPE group was significantly higher than that in MPE group (P < 0.01). (2) LCN-2 mRNA expression in placenta in MPE group and SPE group (0.55 ± 0.14, 0.61 ± 0.14) were both significantly higher than that in control group (0.28 ± 0.16, P < 0.01); LCN-2 protein expression in placenta of MPE group and SPE group (2.2 ± 0.4, 2.4 ± 0.5) were also significantly higher than that in control group (1.4 ± 0.4, P < 0.01), no significant difference was found between MPE group and SPE group (P > 0.05). (3) No significant difference was found in the expressions of NGALR mRNA in placenta among MPE group, SPE group and control group (0.46 ± 0.11, 0.46 ± 0.14, 0.45 ± 0.15, P > 0.05). (4) NGALR protein expressions in MPE group, SPE group and control group were 2.7 ± 0.8, 3.0 ± 0.9, and 2.7 ± 0.9, and there were no significant difference among these three groups (P > 0.05). (5) In preeclampsia, serum LCN-2 level significant associated with 24 hours total urinary protein and uric acid (r = 0.565, 0.476, P < 0.01). LCN-2 serum level were not associated with systolic pressure and diastolic pressure (P > 0.05); there were no association with the expressions LCN-2 mRNA and protein in placenta (P > 0.05). Serum LCN-2 level is closely related to the progress of preeclampsia. Increasing expression of LCN-2 in placenta may be a compensatory response to preeclampsia.

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