Wang Jia-lue, Yang Zi, Wang Rong, Zhu Jin-ming
Department of Obstetric and Gynecology, Peking University Third Hospital, Beijing 100083, China.
Zhonghua Yi Xue Za Zhi. 2008 Jun 3;88(21):1471-5.
To investigate the association of abnormal fatty acid oxidation (FAO), endothelial function activation, and oxidative stress in pathogenesis of severe preeclampsia ( S-PE).
Placenta tissues were obtained from 70 S-PE patients with onset in different gestational weeks with or without liver damage. The protein expression of long chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD), tumor necrosis factor (TNF)-alpha, vascular cell adhesion molecule (VCAM)-1, and peroxisome proliferator activated receptor (PPAR) gamma were analyzed using immunohistochemistry. 54 samples from normal pregnancy in first, second and third trimester were collected as controls.
Protein expression of LCHAD, TNF-alpha, VCAM-1, and PPARgamma could be seen in both placenta of normal pregnancy and S-PE. The protein expression on level of LCHAD of the cases of S-PE that came down of the disease before 32 gestational weeks, especially of the cases complicated with liver damage, was significantly lower than that of the controls (P < 0.05). However, no differences in the LCHAD protein expression were found between the S-PE patients with the onset after and 32 gestational weeks and the controls. The TNF-alpha protein expression levels of the S-PE patients with different onset weeks were all significantly higher than those of the controls (all P < 0.05). The VCAM-1 protein expression levels of the S-PE patients with the onset after 34 gestational weeks was significantly higher than that of the controls (P < 0.05). There was no significant difference in the PPARgamma protein expression between the S-PE patients and the controls. The placental LCHAD protein expression of the S-PE patients with the onset before 32 gestational weeks, especially of the cases with liver function damage, was dramatically decreased in comparison with the controls, and the placental TNF-alpha protein expression was dramatically increased, however, there was no linear correlation between LCHAD and TNF-alpha expression. There was no significant difference in expression of PPARgamma and VCAM-1 between the S-PE patients and the controls. There was no linear correlation among the expression levels of LCHAD, TNF-alpha, VCAM-1, and PPARgamma between the S-PE patients with the onset before and after 32 gestation weeks.
Abnormal FAO may be one of the factors related to some cases of PE with the onset before 32 gestational-weeks, especially those with liver damage. The correlation among LCHAD, TNF-alpha, VCAM-1, and PPARgamma are complicated.
探讨异常脂肪酸氧化（FAO）、内皮功能激活及氧化应激在重度子痫前期（S-PE）发病机制中的关联。
收集70例不同孕周发病的S-PE患者的胎盘组织，其中部分伴有肝损伤，部分不伴有肝损伤。选取54例孕早、中、晚期正常妊娠胎盘组织作为对照。采用免疫组化法分析长链3-羟酰基辅酶A脱氢酶（LCHAD）、肿瘤坏死因子（TNF）-α、血管细胞黏附分子（VCAM）-1及过氧化物酶体增殖物激活受体（PPAR）γ的蛋白表达。
正常妊娠胎盘和S-PE胎盘均可见LCHAD、TNF-α、VCAM-1及PPARγ蛋白表达。孕周<32周发病的S-PE患者，尤其是合并肝损伤者，其胎盘组织中LCHAD蛋白表达水平显著低于对照组（P<0.05）。而孕周≥32周发病的S-PE患者与对照组相比，LCHAD蛋白表达差异无统计学意义。不同孕周发病的S-PE患者TNF-α蛋白表达水平均显著高于对照组（均P<0.05）。孕周≥34周发病的S-PE患者VCAM-1蛋白表达水平显著高于对照组（P<0.05）。S-PE患者与对照组PPARγ蛋白表达差异无统计学意义。孕周<32周发病的S-PE患者，尤其是肝功能损伤者，其胎盘LCHAD蛋白表达较对照组显著降低，胎盘TNF-α蛋白表达显著升高，但LCHAD与TNF-α表达之间无线性相关性。S-PE患者与对照组PPARγ和VCAM-1表达差异无统计学意义。孕周<32周与≥32周发病的S-PE患者LCHAD、TNF-α、VCAM-1及PPARγ表达水平之间无线性相关性。
异常FAO可能是孕周<32周发病的部分PE患者，尤其是合并肝损伤者的发病相关因素之一。LCHAD、TNF-α、VCAM-1及PPARγ之间的相关性较为复杂。
