Role of apoptosis and the expression of bax and bcl-2 on diabetic embryopathy

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Maternal diabetes during pregnancy is associated with increased rate of malformations and growth disturbances in the offspring. Programmed cell death is normally the most common mode of cell death and is present in many developmental processes during morphogenesis. To investigate the role of apoptosis and expression of bax and bcl-2 which promote and inhibit apoptosis on diabetic embryonic malformation, embryos from normal and diabetic mice on day 9,10, and 11 of gestation were examined by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) and immunohistochemical technique. We found: in embryos from normal rats, in primitive gut apoptotic cells were always detected through day 9 to 11, accompanying with strong expression of bax, bcl-2 was expressed in the region where no apoptotic cells. In neural tube and somite, one day 10 and 11, apoptotic cells were detected accompanying with expression of bax in the region; bcl-2 was weakly expressed. In primitive heart, on day 10 and 11, apoptotic cells were rarely detected, and there was strong expression of bax and bcl-2 in the region. In embryos from STZ rats, on day 10 and 11, increased apoptotic cells were detected in primitive gut, neural tube, somite and pharyngealarch. Strong expression of bax and low expression of bcl-2 was observed in the region. In conclusion in diabetic condition increased expression of bax-apoptosis promoting gene-induced abnormal rates of programmed cell death, leading to the loss of the differentiating and migrating cells and has crucial role in congenital malformation in diabetic pregnancy.