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[孕鼠高同型半胱氨酸血症与新生鼠先天性心脏缺陷的关系]

[Relationship of hyperhomocysteinemia in pregnant rats and congenital heart defects in the newborn rats].

作者信息

Lu Yan, Wang Haiqin, Wang Xin

机构信息

Department of Comprehensive Treatment, Hunan Province Maternal and Child Health Hospital, Changsha 410008,China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2011 Jan;36(1):68-73. doi: 10.3969/j.issn.1672-7347.2011.01.011.

Abstract

OBJECTIVE

To investigate the relationship between homocysteine (HCY) and congenital heart defects, and to observe the toxic effect of different doses of HCY on embryonic heart development in mammalian.

METHODS

A total of 30 SD pregnant rats were randomly divided into 3 groups: a high dose group [200 mg/(kg.d)], a low dose group [(100 mg/(kg.d)] and a control group (equal volume of physiologic saline, n=10 in each group). The HCY or vehicle was given intraperitoneally from 7 to 20 days after uterineincision delivery. The contents of HCY in serum were analyzed by high performance liquid chromatogram electrochem before the pregnancy and 20 days after the pregnancy. The structure changes of the newborn rats heart were observed by stereoscope. The ultrastructure changes of cadiomyocyte were observed through transmission electron microscope.

RESULTS

Comparing with the control, serum HCY in rats 20 days after pregnancy was significantly increased in the high or low dose group [(30.47 ± 1.12), (20.90 ± 1.08)vs(10.98 ± 0.77)μmol/L, P<0.01)], indicating that the hyperhomocysteinemia animal model was successfully established. The incidence rate of congenital heart defects in neonatal was significantly increased in the high or low dose group(14.13%, 9.57% vs 0.76%, P<0.01). The number of apoptotic cells were significantly increased in the high dose group.

CONCLUSION

Hyperhomocysteinemia may exert toxic effect on embryonic heart development in pregnancy rats, which led to congenital heart defects in the newborn rats. Hyperhomocysteinemia induced cardiomyocyte apoptosis may, at least partially, contribute to the heart defects.

摘要

目的

探讨同型半胱氨酸(HCY)与先天性心脏缺陷之间的关系,并观察不同剂量的HCY对哺乳动物胚胎心脏发育的毒性作用。

方法

将30只SD孕鼠随机分为3组:高剂量组[200mg/(kg·d)]、低剂量组[100mg/(kg·d)]和对照组(等体积生理盐水,每组10只)。于子宫切开分娩后7至20天腹腔注射HCY或赋形剂。在妊娠前和妊娠20天后,通过高效液相色谱电化学法分析血清中HCY的含量。用体视显微镜观察新生大鼠心脏的结构变化。通过透射电子显微镜观察心肌细胞的超微结构变化。

结果

与对照组相比,高剂量组和低剂量组妊娠20天后大鼠血清HCY显著升高[(30.47±1.12),(20.90±1.08)vs(10.98±0.77)μmol/L,P<0.01],表明成功建立了高同型半胱氨酸血症动物模型。高剂量组和低剂量组新生大鼠先天性心脏缺陷的发生率显著增加(14.13%,9.57% vs 0.76%,P<0.01)。高剂量组凋亡细胞数量显著增加。

结论

高同型半胱氨酸血症可能对妊娠大鼠胚胎心脏发育产生毒性作用,导致新生大鼠先天性心脏缺陷。高同型半胱氨酸血症诱导的心肌细胞凋亡可能至少部分导致心脏缺陷。

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