目的 探讨血清及胎盘中脂蛋白相关磷脂酶A2(Lp-PLA2)与妊娠期高血压疾病的关系。方法 采用酶联免疫吸附法及免疫组织化学方法检测60例妊娠期高血压疾病患者(妊娠高血压19例、轻度子痫前期25例、重度子痫前期16例) 及20例正常妊娠妇女(对照组)血清及胎盘中Lp-PLA2水平,并分析其与妊娠期高血压疾病的关系。结果 妊娠期高血压疾病组胎盘中Lp-PLA2表达水平明显高于对照组(P<0.05)。轻度子痫前期组Lp-PLA2表达水平显著高于对照组(P<0.05),重度子痫前期Lp-PLA2表达水平显著高于轻度子痫前期组(P<0.05)。妊娠期高血压疾病组血清中Lp-PLA2水平显著高于对照组(P<0.05)。随着病情的加重,Lp-PLA2水平呈逐渐上升趋势,对照组、妊娠高血压、轻度子痫前期、重度子痫前期每两组之间比较,差异均有统计学意义(P均<0.05)。妊娠期高血压疾病组血清与胎盘中Lp-PLA2水平呈正相关(r=0.435,P<0.05)。结论 Lp-PLA2水平的升高可能与妊娠期高血压疾病的发生有关,母血中Lp-PLA2水平的变化有可能作为疾病的监测指标。
Abstract
Objective To investigate the relationship between Lp-PLA2 levels in maternal serum and placenta and hypertensive disorders of pregnancy. Methods The levels of Lp-PLA2 in serum and placenta of 60 patients with hypertensive disorders of pregnancy (19 cases of gestational hypertension, 25 cases of mild preeclampsia, and 16 cases of severe preeclampsia) and 20 normal pregnant women (control group) were measured by enzyme-linked immunosorbent assay and immunohistochemistry. The relationship between levels of Lp-PLA2 and hypertensive disorders of pregnancy was analyzed. Results 1) The expression level of Lp-PLA2 in placenta of patients with hypertensive disorders of pregnancy was significantly higher than that of the control group (P<0.05), so was the expression level of Lp-PLA2 in the mild preeclampsia group (P<0.05). The level in the severe preeclampsia group was significantly higher than that of the mild preeclampsia group (P<0.05). 2) The level of maternal serum Lp-PLA2 was significantly higher than that of the control group(P<0.05). With the aggravation of the disease, the level of Lp-PLA2 increased gradually. There was significant difference between the two groups (all P<0.05). 3) There was a positive correlation between the levels of Lp-PLA2 in serum and in placenta of patients with hypertensive disorders of pregnancy (r=0.435, P< 0.05). Conclusions The increase of Lp-PLA2 levels may be related to the occurrence of hypertensive disorders of pregnancy. The change of Lp-PLA2 levels in maternal serum may be used as a monitoring indicator of the disease.
关键词
脂蛋白相关磷脂酶A2 /
妊娠期高血压疾病 /
酶联免疫吸附法 /
免疫组织化学方法
Key words
Lp-PLA2 /
hypertensive disorders of pregnancy /
enzyme-linked immuno sorbent assay /
immunohistochemistry
{{custom_sec.title}}
{{custom_sec.title}}
{{custom_sec.content}}
参考文献
[1] Tarca A L, Romero R, Benshalom T N, et al. The prediction of early preeclampsia: results from a longitudinal proteomics study [J]. PLoS One, 2019, 14(6): e0217273.
[2] Jia K, Ma L J, Wu S Y, et al. Serum levels of complement factors C1q, Bb, and H in normal pregnancy and severe Pre-Eclampsia [J]. Med Sci Monit, 2019, 25(9): 7087-7093.
[3] Tomimatsu T, Mimura K, Matsuzaki S, et al. Preeclampsia: maternal systemic vascular disorder caused by generalized endothelial dysfunction due to placental antiangiogenic factors [J]. Int J Mol Sci, 2019, 20(17): 4246-4264.
[4] Olaoye T, Oyerinde O O, Elebuji O J, et al. Knowledge, perception and management of pre-eclampsia among health care providers in a maternity hospital [J]. Int J MCH AIDS, 2019, 8(2): 80-88.
[5] Alahakoon T I, Medbury H J, Williams H, et al. Lipid profiling in maternal and fetal circulations in preeclampsia and fetal growth restriction-a prospective case control observational study [J]. BMC Pregnancy Childbirth, 2020, 20(1): 61-71.
[6] Tenório M B, Ferreira R C, Moura F A, et al. Cross-Talk between oxidative stress and inflammation in preeclampsia[J].Oxid Med Cell Longev, 2019, 2019(11): 8238727-8238753.
[7] Huang F B, Wang K, Shen J H. Lipoprotein-associated phospholipase A2: The story continues [J]. Med Res Rev, 2020, 40(1): 79-134.
[8] Jackisch L, Kumsaiyai W, Moore J D, et al. Differential expression of Lp-PLA2 in obesity and type 2 diabetes and the influence of lipids [J]. Diabetologia, 2018 ,61(5): 1155-1166.
[9] 谢 幸. 妇产科学[M]. 9版. 北京:人民卫生出版社. 2018:83-91.
[10] Siddiqui M K, Kennedy G, Carr F, et al. Lp-PLA2 activity is associated with increased risk of diabetic retinopathy: a longitudinal disease progression study [J]. Diabetologia, 2018, 61(6): 1344-1353.
[11] Li J W, Wang H, Tian J, et al. Change in lipoprotein-associated phospholipase A2 and its association with cardiovascular outcomes in patients with acute coronary syndrome [J]. Medicine (Baltimore), 2018, 97(28): e11517.
[12] Chen B F, Deng Y, Xu X, et al. Effect of selective thrombus aspiration on serum lipoprotein-associated phospholipase A2 in Patients with ST-Elevation myocardial infarction undergoing primary percutaneous coronary intervention with high thrombus burden [J]. Acta Cardiol Sin, 2018, 34(3): 233-241.
[13] Tian Y, Jia H, Li S, et al. The associations of stroke, transient ischemic attack, and/or stroke-related recurrent vascular events with Lipoprotein-associated phospholipase A2: a systematic review and meta-analysis [J]. Medicine (Baltimore), 2017, 96(51): e9413.
[14] Cao J, Hsu Y H, Li S, et al. Structural basis of specific interactions of Lp-PLA2 with HDL revealed by hydrogen deuterium exchange mass spectrometry [J]. J Lipid Res, 2013, 54(1): 127-133.
[15] Paik J K, Kim M, Kim M, et al. Circulating Lp-PLA2 activity correlates with oxidative stress and cytokines in overweight/obese postmenopausal women not using hormone replacement therapy [J]. Age (Dordr) , 2015, 37(2): 32-42.
[16] He S, Chousterman B G, Fenn A, et al. Lp-PLA2 antagonizes left ventricular healing after myocardial infarction by impairing the appearance of reparative macrophages [J]. Circ Heart Fail, 2015, 8(5): 980-987.
[17] Balc E Ö, Ekmekçi H, Güngör Z, et al. Evaluation of Lp-PLA2 mass, vitronectin and PAI-1 activity levels in patients with preeclampsia [J]. Arch Gynecol Obstet, 2015, 292(1):53-58.
[18] 洪 岩. Lp-PLA2与妊娠期高血压疾病的关系及其临床意义研究[D]. 吉林:吉林大学, 2015:1-31.
[19] Dhamoon M S, Cheung Y K, Moon Y P, et al. Interleukin-6 and lipoprotein-associated phospholipase A2 are associated with functional trajectories [J]. PLoS One, 2019,14(4):e0214784.
[20] Güngör Z B, Tüten A, Ekmekçi H, et al. Possible effects of lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms on cardiovascular risk in patients with preeclampsia [J]. J Matern Fetal Neonatal Med, 2018, 31(23):3119-3127.