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目的研究维甲酸诱导形成大鼠肛门直肠畸形的胚胎发育过程和α-SMA表达模式,探讨肛门直肠畸形矫正术后便秘和便失禁产生的原因。方法利用ATRA诱导大鼠产生肛门直肠畸形胚胎,病理形态学方法观察对比妊娠12、13、14、16、18d时大鼠胚胎肠道系统发育过程,并且通过免疫组化染色进行α-SMA表达的检测,与对照组胚胎中α-SMA表达表达模式进行对比。结果实验组中80%胚胎具有肛门直肠畸形,对照组未见明显畸形。胚胎发育观察证实妊娠12～16d为肛门形成的关键时间,畸形组与对照组相比发育明显滞后而且机构异常,α-SMA表达强度随胎龄增加,与肠道系统分化程度同步,畸形组中表达区域分散且未见外括约肌部分表达分布。结论 ATRA诱导产生无肛畸形胚胎中肠道系统发育过程与α-SMA表达同步相关,畸形组括约肌部分发育异常和α-SMA表达异常可能是肛门直肠畸形矫正术后便秘和便失禁产生的原因。
Objective To study the embryonic development and α-SMA expression induced by retinoic acid in rats with anorectal malformation and to explore the causes of constipation and incontinence after anorectal deformity correction. Methods ATRA-induced anorectal malformation embryos were made in rats. Pathological morphological observation was used to observe the development of intestinal system in rat embryos at 12, 13, 14, 16 and 18 days. The expression of α-SMA was detected by immunohistochemical staining The expression of α-SMA in control group was compared with that in control group. Results 80% of the embryos in the experimental group had anorectal malformations and no obvious deformity in the control group. The observation of embryo development confirmed that the critical time for anus formation was between 12 and 16 days of gestation. The deformity group developed obviously lag and the organization was abnormal compared with the control group. The expression of α-SMA increased with gestational age and synchronously with the degree of intestinal system differentiation. Disseminated expression area and no external sphincter part of the expression distribution. Conclusions ATRA-induced anorexia-deformed embryos develop synchronously with the expression of α-SMA, and the abnormal development of sphincter and the abnormal expression of α-SMA may be responsible for constipation and incontinence in anorectal malformations.