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目的观察坏死性小肠结肠炎(NEC)新生鼠肠道组织中Caspase-3和ki67的表达情况,探讨谷氨酰胺(Gln)对NEC新生鼠肠道的保护作用及可能机制。方法 30只早产鼠(21d)及30只足月新生鼠分别分为早产模型组、早产Gln干预组、早产对照组、足月模型组、足月Gln干预组和足月对照组。代乳品人工喂养+缺氧+冷刺激建立NEC模型,Gln干预组采用代乳品+Gln人工喂养,同时予缺氧冷刺激;对照组置于(代)母鼠身旁喂养,不进行任何干预。第3天处死后取出大鼠肠道,HE染色后对其回肠进行病理评分,免疫组织化学检测其空肠、回肠及结肠Caspase-3和ki67的表达。采用SPSS13.0软件进行统计学分析。结果与对照组比较,模型组空肠、回肠及结肠病理评分、Caspase-3和ki67的表达均增加(Pa<0.01);与模型组比较,Gln干预组上述指标的改变得到显著改善(Pa<0.05);早产鼠模型组、Gln干预组及对照组空肠、回肠、结肠病理评分、Caspase-3和ki67的表达分别与对应的足月鼠模型组、Gln干预组及对照组比较,差异均无统计学意义(Pa>0.05)。结论细胞凋亡与增殖参与了NEC的病变过程,Gln对肠道的保护作用可能是通过调控凋亡与增殖的平衡来实现的。
Objective To observe the expression of Caspase-3 and ki67 in the necrotic enterocolitis (NEC) neonatal rat intestine and to explore the protective effect of glutamine (Gn) on the intestinal tract of neonatal rats with NEC and its possible mechanism. Methods Thirty preterm rats (21d) and 30 term newborn rats were divided into preterm model group, preterm preterm Gln group, preterm control group, term model group, full term Gln intervention group and term control group. NEC model was established by artificial feeding + hypoxia + cold stimulation in lactating dairy cow. Gln intervention group was fed with milk substitute + Gln while stimulated by hypoxia. Control group was placed beside (on) mother rats without any intervention. The rats were sacrificed on day 3, and the intestines of rats were removed. The pathological scores of ileum were detected by HE staining. The expressions of Caspase-3 and ki67 in jejunum, ileum and colon were detected by immunohistochemistry. SPSS13.0 software was used for statistical analysis. Results Compared with the control group, the expression of Caspase-3 and Ki67 in jejunum, ileum and colon increased (P <0.01) in the model group, while the changes of the above indexes in the model group were significantly improved (P <0.05 ). The expressions of Caspase-3, Ki-67 and jejunum, ileum and colon in preterm model group, Gln group and control group were not statistically different from those in corresponding model group, Gln group and control group Significance (Pa> 0.05). Conclusion Apoptosis and proliferation are involved in the pathological process of NEC. The protective effect of Gln on the intestine may be achieved by regulating the balance between apoptosis and proliferation.