Zhu X D, Bonet B, Knopp R H
Northwest Lipid Research Clinic, Department of Medicine, University of Washington School of Medicine, Seattle 98104, USA.
Am J Obstet Gynecol. 1997 Jul;177(1):196-209. doi: 10.1016/s0002-9378(97)70462-9.
We have previously shown that low-density lipoprotein oxidation is diminished by 17beta-estradiol and enhanced by progesterone and testosterone. In these experiments we wished to learn whether sex hormone effects on low-density lipoprotein oxidation alter placental cell viability in primary tissue culture.
Primary tissue culture of human term placental cells was performed.
Addition of 17beta-estradiol decreased low-density lipoprotein oxidation (measured as lipid peroxides, thiobarbituric acid-reacting substances, and low-density lipoprotein electrophoretic mobility) and placental cell toxicity (measured as chromium 51 release) with maximum reductions of 28% (macrophages) (p < 0.05) and 26% (trophoblasts) (p < 0.01). Conversely, progesterone and testosterone increased low-density lipoprotein oxidation and chromium 51 release, the latter a maximum of 28% and 18%, respectively, for progesterone and testosterone in macrophages (p < 0.05 in both instances) and 23% in trophoblasts (p < 0.05, testosterone only). Collectively, cytotoxicity was proportional to low-density lipoprotein oxidation and estradiol, progesterone, and testosterone concentrations.
Estradiol inhibits placental macrophage- and trophoblast-mediated low-density lipoprotein oxidation and cytotoxicity, whereas progesterone and testosterone promote these effects. Sex steroid hormones may modulate the effects of oxidative stress on placental function in pregnancy.
我们之前已经表明，低密度脂蛋白氧化可被17β-雌二醇减少，并被孕酮和睾酮增强。在这些实验中，我们希望了解性激素对低密度脂蛋白氧化的影响是否会改变原代组织培养中胎盘细胞的活力。
进行了人足月胎盘细胞的原代组织培养。
添加17β-雌二醇可降低低密度脂蛋白氧化（以脂质过氧化物、硫代巴比妥酸反应物质和低密度脂蛋白电泳迁移率衡量）以及胎盘细胞毒性（以51铬释放衡量），巨噬细胞最大降低28%（p<0.05），滋养层细胞最大降低26%（p<0.01）。相反，孕酮和睾酮增加低密度脂蛋白氧化和51铬释放，巨噬细胞中孕酮和睾酮分别最大增加28%和18%（两种情况p均<0.05），滋养层细胞中睾酮最大增加23%（p<0.05，仅睾酮）。总体而言，细胞毒性与低密度脂蛋白氧化以及雌二醇、孕酮和睾酮浓度成正比。
雌二醇抑制胎盘巨噬细胞和滋养层细胞介导的低密度脂蛋白氧化和细胞毒性，而孕酮和睾酮则促进这些作用。性类固醇激素可能调节氧化应激对妊娠中胎盘功能的影响。
