Department of Gynaecology and Obstetrics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Department of Gynaecology and Obstetrics, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, Zhejiang, China.
Placenta. 2018 Feb;62:16-24. doi: 10.1016/j.placenta.2017.12.004. Epub 2017 Dec 7.
Preeclampsia is associated with the presence of pathogenic angiotensin-receptor-activating autoantibodies. Cadmium is an increasingly prevalent environmental pollutant that can mimic oestrogens, which may enhance immunoglobulin production. Progesterone exerts opposite effects to oestrogen.
We measured the levels of cadmium and progesterone in preeclamptic patients and controls. Pregnant rats exposed to cadmium (0.125 mg/kg body weight) from gestational day 9-12 were treated with/without progesterone (3 mg/kg) beginning from gestational day 9 to delivery. We analysed the main features of preeclampsia and circulating level of the angiotensin II type 1 receptor agonistic autoantibody. We also measured the expression of activation-induced cytosine deaminase in B cells.
There were higher cadmium levels and lower progesterone levels in the blood of preeclamptic women than in the blood of those with a healthy pregnancy. Based on this finding, a rat model of preeclampsia was established by intraperitoneally administrating low-dose cadmium on gestational days 9-12. Rats were then treated with/without progesterone. Key features of preeclampsia, including hypertension, proteinuria and placental abnormalities, appeared in pregnant rats after cadmium injection and improved after treatment with progesterone. Cadmium increased immunoglobulin production, mainly angiotensin II type 1-receptor-agonistic autoantibodies, by increasing the expression of activation-induced cytosine deaminase in B cells; progesterone exerted an opposite effect.
Cadmium induced immune abnormalities that may be a key pathogenic contributor to preeclampsia. Progesterone supplementation to correct hormonal imbalance may be a viable strategy for preeclampsia management.
子痫前期与致病性血管紧张素受体激活自身抗体的存在有关。镉是一种日益流行的环境污染物,它可以模拟雌激素,从而增强免疫球蛋白的产生。孕激素对雌激素产生相反的作用。
我们测量了子痫前期患者和对照组的镉和孕酮水平。从妊娠第 9 天到第 12 天,给暴露于镉(0.125mg/kg 体重)的妊娠大鼠用/不用孕激素(3mg/kg)治疗,从妊娠第 9 天到分娩。我们分析了子痫前期的主要特征和血管紧张素 II 型 1 受体激动性自身抗体的循环水平。我们还测量了 B 细胞中激活诱导胞嘧啶脱氨酶的表达。
与健康妊娠的孕妇相比,子痫前期妇女的血液中镉水平较高,孕酮水平较低。基于这一发现,我们通过在妊娠第 9-12 天腹腔内给予低剂量镉建立了子痫前期大鼠模型。然后,用/不用孕激素治疗大鼠。在注射镉后,妊娠大鼠出现了子痫前期的关键特征,包括高血压、蛋白尿和胎盘异常,用孕激素治疗后得到改善。镉通过增加 B 细胞中激活诱导胞嘧啶脱氨酶的表达来增加免疫球蛋白的产生,主要是血管紧张素 II 型 1 受体激动性自身抗体;孕激素则产生相反的作用。
镉引起的免疫异常可能是子痫前期的一个关键致病因素。补充孕激素以纠正激素失衡可能是子痫前期治疗的一种可行策略。