p53、bcl-2和bax基因表达与IUGR胎盘细胞凋亡的相关性研究

目的：研究胎儿宫内发育迟缓（ｉｎｔｒａｕｔｅｒｉｎｅ　ｇｒｏｗｔｈ　ｒｅｔａｒｄａｔｉｏｎ，ＩＵＧＲ)患者的胎盘细胞凋亡，以ｐ５３、ｂｃｌ－２和ｂａｘ相关性。方法：收集ＩＵＧＲ ２０份和正常足月分娩１２例的胎盘组织，应用原位末端标记(TUNEL)法检测其胎盘组织中的细胞凋亡，免疫组化法（ＩＨＣＡ）检测胎盘组织中ｐ５３、ｂｃｌ－２和ｂａｘ基因表达。结果：①正常和ＩＵＧＲ胎盘组织中均可见凋亡细胞，但ＩＵＧＲ胎盘中细胞凋亡指数（ａｐｏｐｔｏｓｉｓ　ｉｎｄｅｘ，ＡＩ）为１６．７～６８．３１，明显高于正常胎盘中的９．２～３０．４／高倍视野（平均２０．６７／高倍视野），差异有显著性（Ｐ＜０．０５）；②ＩＵＧＲ ２０例胎盘组织中均有ｂａｘ过表达（４０％～９０％)，高于正常组织（１０％～４０％），差异有显著性（Ｐ＜０．０５）；③正常及ＩＵＧＲ胎盘组织中均未见ｂｃｌ－２表达；④ｐ５３在ＩＵＧＲ胎盘组织中的表达为５０％～８０％，而在正常组织中为５５％～８０％（Ｐ＞０．０５）；⑤ＩＵＧＲ２０例胎盘组织中细胞ＡＩ与ｂａｘ的表达呈正相关，与ｐ５３表达无关，ｂａｘ与ｐ５３之间无相关性。结论：①正常孕妇和ＩＵＧＲ患者胎盘组织中均有细胞凋亡，但ＩＵＧ

Study on the relationship between p53,bcl-2,bax expressions and cell apoptosis in placenta with intrauterine growth retardaton

Objective:To study on the relationship between p53、bcl-2,b ax expressions and cell apoptosis inplac enta with fetal intrauterine growth reta rdation(IUGR).Methods :20 placental sample with IUGR and 1 2 normal placental sample of third-trime ster pregnancies were collected.TUNEL(Td T-mediated dUTP nick end labeling) assay was used for evaluating the cells apop tosis index (AI),and LSAB(labeled strept avidin biotin) immunohistochemical metho d was adopted to detect the bcl-2 bax an d p53 expression,in normal and IUGR placenta tissues.Results:①Cell apoptosis could be found both in normal and IUGR placental tissues.The AI of IUG R group was 16.7 68.3/high power field(H PV),46.55/HPF averagely,which was signif icantly higher than that of normal group (9.2～30.4/HPF,20.67/HPF averagely)(P<0.05).②Bax overexpressed in 20 IUGR placental tissues(40%～90%),it was significantly higher than that of normal tissues (P<0.05).③Bcl-2 could not be detected in IUGR or normal placental t issues.④50%～80% palcental cell expressed p53 in IUGR,and 55%～80% in normal group ,there was on significant different(P>0.05).⑤There existed positive correlation between AI and bax in IUGR.Ho wever,the AI did not correlate with p53, and there was no correlation between bax and p53.Conclusions:①Cell apopt osis exists both in normal and IU GR placental tissues,but increased the c ell apoptosis in IUGR is a prim ary pathologi c process that results in IUGR.②The apop tosis developed in IUGR is highly probab le through a p53- independent and bax-mediated pathway.③Th e hypoxia/ischemia is a critical factor result in overexpression of bax.