Objective: To explore the correlation between severe preeclampsia and abnormal expression of long-chain 3-hydroxyacyl-CoA dehydrogenase (LCHAD).
Methods: Serum-free trophoblast cells cultured in vitro were divided into 4 groups under the stimulations of normal pregnancy serum (NP group), early onset severe preeclampsia serum (E-PE group), late onset severe preeclampsia serum (L-PE group) and HELLP (hemolysis, elevated liver enzymes & low platelets) syndrome serum (HELLP group) respectively. The expressions of mRNA and protein of LCHAD in trophoblast cells were detected by real-time polymerase chain reaction (PCR) and Western blot.
Result: (1) Expression of LCHAD mRNA: the relative expressions of mRNA of LCHAD in NP, E-PE, L-PE and HELLP groups were 1.00 ± 0.00, 3.08 ± 0.22, 1.62 ± 0.23 and 3.36 ± 0.18 respectively. The relative expressions of LCHAD mRNA were significantly reduced in the E-PE, L-PE and HELLP groups versus the NP group (P < 0.05). Compared with the L-PE group, the gene expressions of LCHAD significantly decreased in the E-PE and HELLP groups (P < 0.05) while no significant difference was found between the E-PE and HELLP groups (P > 0.05). (2) Expression of LCHAD protein: the relative expressions of LCHAD protein were 4.94 ± 0.02, 2.93 ± 0.13, 4.14 ± 0.06 and 2.80 ± 0.09 in the NP, E-PE, L-PE and HELLP groups respectively. The protein expressions of LCHAD were remarkably reduced in the E-PE, L-PE and HELLP groups versus the NP group (P < 0.05). The expressions of LCHAD protein remarkably decreased in the E-PE and HELLP groups versus the L-PE group (P < 0.05) while no significant difference was found between the E-PE and HELLP groups (P > 0.05).
Conclusion: Long chain fatty acid oxidation is involved in the pathogenesis and development of preeclampsia. The expressions of LCHAD gene and protein are remarkably affected by early onset severe preeclampsia and HELLP syndrome. The interacting mechanism and influence between fatty acid oxidation and the development of preeclampsia are worth further exploring.
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