Objective: To investigate the association of abnormal fatty acid oxidation (FAO), endothelial function activation, and oxidative stress in pathogenesis of severe preeclampsia ( S-PE).
Methods: 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.
Results: 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.
Conclusion: 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.