| Chen HW |
------>authors3_c=None ------>paper_class1=1 ------>Impact_Factor=3.170 ------>paper_class3=2 ------>paper_class2=1 ------>vol=75 ------>confirm_bywho=tzengcr ------>insert_bywho=tzengcr ------>Jurnal_Rank=7.3 ------>authors4_c=None ------>comm_author=1 ------>patent_EDate=None ------>authors5_c=None ------>publish_day=None ------>paper_class2Letter=None ------>page2=1171 ------>medlineContent= ------>unit=E0111 ------>insert_date=20051213 ------>iam=3 ------>update_date=None ------>author=??? ------>change_event=4 ------>ISSN=None ------>authors_c=None ------>score=454 ------>journal_name=Fertil Steril. ------>paper_name=Nitric oxide as regulator in preimplantation embryo development and apoptosis. ------>confirm_date=20051217 ------>tch_id=079009 ------>pmid=11384644 ------>page1=1163 ------>fullAbstract=OBJECTIVE: To investigate the mechanisms of nitric oxide (NO) in the development and apoptosis of preimplantation mouse embryos. DESIGN: Prospective, controlled study. SETTING: Medical college laboratory. SUBJECT(S): Two-cell embryos from outbred ICR mice. INTERVENTION(S): Hyperstimulation protocol, two-cell embryos were collected, then treated with or without an NO synthase inhibitor (L-NAME) or an NO donor (SNP) and combined with a cGMP analogue (8-Br-cGMP) or a selective inhibitor of NO-sensitive soluble guanylyl cyclase (ODQ). MAIN OUTCOME MEASURE(S): The development of ICR mouse embryo from two cells to blastocyst stages in vitro. RESULT(S): The development of blastocyst was inhibited by L-NAME in a concentration-dependent manner (0.1-10 microM) and 0.1 microM SNP reversed this effect (80.5% of control). Annexin-V/propidium iodide and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling techniques demonstrated that excessive NO (> or =10 microM) might induce apoptosis in the mouse embryos. 8-Br-cGMP reversed the inhibitory effect of L-NAME and rescued the embryo growth. ODQ inhibited the embryo development in a dose-responsive fashion (0.1--100 microM) but had no effect in the NO-induced embryo apoptosis. P53 and Bax were found to be up-regulated during the embryo fragmentation. CONCLUSION(S): These results indicate that the cGMP pathway might be involved in the NO-regulated embryonic development, but not in NO-induced apoptosis, for which P53/Bax pathway might be involved. ------>tmu_sno=None ------>sno=12234 ------>authors2=Jiang WS ------>authors3=Tzeng CR ------>authors4= ------>authors5= ------>authors6= ------>authors6_c=None ------>authors=Chen HW ------>delete_flag=0 ------>SCI_JNo=None ------>authors2_c=None ------>publish_area=None ------>updateTitle=Nitric oxide as a regulator in preimplantation embryo development and apoptosis. ------>language=2 ------>check_flag=None ------>submit_date=None ------>country=None ------>no= ------>patent_SDate=None ------>update_bywho=None ------>publish_year=2001 ------>submit_flag=None ------>publish_month=None |