摘要
Background Experimental evidence indicates that cyclooxygenase-2 （COX-2） plays a critical role in blastocyst implantation; however, little is known of the role of COX-2 in unexplained recurrent spontaneous abortion （URSA）. Methods We evaluated the expression level and potential signaling pathway of COX-2 in 30 cases of URSA who were excluded the abnormality of chromosomes, anatomy, endocrine, infectious, autoimmune diseases and in 30 normal pregnancies. Results The mRNA and the protein expression level of COX-2 in the URSA group （-0.238±0.848, 0.368±0.089, respectively） were significantly lower than that in the control group （1.943±3.845, 1.046±0.108, respectively） （both, P 〈0.01）. The expression of prostaglandins PGF2a, PGD2, PGE2, and PGI2, in the URSA group （（2326.0±295.6） pg/ml, （2164.0±240.5） pg/ml, （238.7±26.4） pg/ml, （2337.0±263.0） pg/ml, respectively） were significantly lower than that in the control group （（3450.0±421.7） pg/ml, （3174.0±415.6） pg/ml, （323.5±43.8） pg/ml, （3623.0±460.4） pg/ml, respectively） （P 〈0.05）. The mRNA expression level of PPARI3 and RXRa （0.859±0.653, -0.172±0.752, respectively） in URSA group was significantly lower than that in the control group （1.554±1.735, 0.777±2.482, respectively） （both P 〈0.05）. The mRNA and protein expression levels of vascular endothelial growth factor-A （VEGF-A） in the URSA group （2.010±1.522, 0.35±0.46） was significantly lower than that in the control group （4.569±2.430, 0.750±0.350） （both P 〈0.05）. Conclusions COX-2 and the COX-2-derived PGI2 signaling pathway possibly play an important role in successful embryo implantation, and their decreased expression may result in URSA. The decreased expression may influence the expression of VEGF-A which interferes with placental angiogenesis causing failure of embryo implantation, leading to spontaneous abortion.
Background Experimental evidence indicates that cyclooxygenase-2 （COX-2） plays a critical role in blastocyst implantation; however, little is known of the role of COX-2 in unexplained recurrent spontaneous abortion （URSA）. Methods We evaluated the expression level and potential signaling pathway of COX-2 in 30 cases of URSA who were excluded the abnormality of chromosomes, anatomy, endocrine, infectious, autoimmune diseases and in 30 normal pregnancies. Results The mRNA and the protein expression level of COX-2 in the URSA group （-0.238±0.848, 0.368±0.089, respectively） were significantly lower than that in the control group （1.943±3.845, 1.046±0.108, respectively） （both, P 〈0.01）. The expression of prostaglandins PGF2a, PGD2, PGE2, and PGI2, in the URSA group （（2326.0±295.6） pg/ml, （2164.0±240.5） pg/ml, （238.7±26.4） pg/ml, （2337.0±263.0） pg/ml, respectively） were significantly lower than that in the control group （（3450.0±421.7） pg/ml, （3174.0±415.6） pg/ml, （323.5±43.8） pg/ml, （3623.0±460.4） pg/ml, respectively） （P 〈0.05）. The mRNA expression level of PPARI3 and RXRa （0.859±0.653, -0.172±0.752, respectively） in URSA group was significantly lower than that in the control group （1.554±1.735, 0.777±2.482, respectively） （both P 〈0.05）. The mRNA and protein expression levels of vascular endothelial growth factor-A （VEGF-A） in the URSA group （2.010±1.522, 0.35±0.46） was significantly lower than that in the control group （4.569±2.430, 0.750±0.350） （both P 〈0.05）. Conclusions COX-2 and the COX-2-derived PGI2 signaling pathway possibly play an important role in successful embryo implantation, and their decreased expression may result in URSA. The decreased expression may influence the expression of VEGF-A which interferes with placental angiogenesis causing failure of embryo implantation, leading to spontaneous abortion.
