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目的:观察叶酸对妊娠大鼠心肌细胞凋亡及Bax、Bcl-2蛋白表达的影响,在细胞水平探讨叶酸预防先天性心脏畸形的作用及机制,为临床应用叶酸预防出生缺陷性疾病提供理论和实验依据。方法:成年雌性SD大鼠40只,随机分为对照组、大、中、小剂量叶酸组。叶酸组受孕后灌胃给予2、1、0.5mg/kg/d等不同剂量叶酸,自受孕日开始持续10天。ED13.5天处死大鼠并取胎鼠心脏,常规制备组织切片,免疫组化检测Bax、Bcl-2的表达情况,TUNEL法检测细胞凋亡率。结果:与对照组比较,叶酸干预组的细胞凋亡率、Bax表达均明显降低(P<0.01),Bcl-2的表达显著增高(P<0.05);叶酸不同剂量组间比较,Bax和Bcl-2蛋白表达、细胞凋亡率在大、中剂量组与小剂量组差异显著(P<0.05),大剂量组与中剂量组比较差异无统计学意义(P>0.05)。结论:叶酸干预可降低胎鼠心肌细胞的凋亡率和Bax的表达,提高Bcl-2的表达。一定范围内,叶酸对Bax、Bcl-2表达及细胞凋亡率的影响与剂量有关联。叶酸抑制心脏细胞凋亡的作用可能与预防畸形的作用机制有关。
OBJECTIVE: To observe the effect of folic acid on the apoptosis of myocardial cells and the expression of Bax and Bcl-2 in pregnant rats, to explore the effect and mechanism of folic acid on prevention of congenital heart defects at the cellular level, to provide theoretical and theoretical basis for the clinical application of folic acid in preventing birth defects. Experimental basis. Methods: Forty adult female Sprague-Dawley rats were randomly divided into control group, large, medium and small doses of folic acid group. Folate group after conception by gavage given 2,1,0.5 mg / kg / d and other different doses of folic acid, since the conception day for 10 days. The rats were sacrificed on day 13 and fetus hearts were taken out. Tissue sections were prepared routinely. Immunohistochemistry was used to detect the expression of Bax and Bcl-2. TUNEL method was used to detect the apoptosis rate. Results: Compared with the control group, the apoptosis rate and the expression of Bax were significantly decreased (P <0.01) and the expression of Bcl-2 was significantly increased in the folic acid intervention group (P <0.05) (P <0.05). There was no significant difference between the high-dose group and the medium-dose group (P> 0.05) .2. Conclusion: Folic acid intervention can reduce the apoptosis rate of fetal rat cardiomyocytes and Bax expression, increase Bcl-2 expression. Within a certain range, the effect of folic acid on Bax, Bcl-2 expression and apoptosis rate was related to dose. Folic acid inhibition of cardiac apoptosis may be related to the mechanism of prevention of deformity.