论文部分内容阅读
目的动态观察新生大鼠坏死性小肠结肠炎(NEC)发病过程中肠组织一氧化氮(NO)含量、一氧化氮合酶(NOS)活性变化及其与肠损伤关系,为进一步阐明NEC发病机制、寻找新的治疗方法提供实验依据。方法40只新生SD大鼠按简单随机法分成模型组(M)32只,对照组(C)8只。模型组大鼠出生48h开始鼠配方奶人工喂养,并予以3次缺氧和冷刺激建立NEC模型,缺氧冷刺激开始后24h(M24)、48h(M48)、72h(造模结束,M72)及最后一次缺氧和冷刺激后24h(M96)分别空腹断头处死8只;实验结束时处死对照组大鼠,分别留取肠管进行肠组织损伤评分、肠组织中NO含量和NOS活性检测。结果建模后,模型组出现腹泻、腹胀、萎靡、活动减少。M24、M48、M72、M96及对照组肠组织损伤评分分别为(1.25±0.56)、(1.46±0.31)、(2.79±0.40)、(3.33±0.59)和(0.08±0.15)分,肠组织NO含量分别为(2.07±0.38)、(2.88±0.32)、(3.09±0.40)、(3.98±1.15)和(0.94±0.44)μmol/gprot,总NOS活性分别为(2.21±0.42)、(2.77±0.58)、(2.95±0.32)、(3.80±1.08)和(1.49±0.25)U/mgprot,诱导型NOS活性为(1.25±0.27)、(1.94±0.46)、(2.06±0.18)、(2.86±1.07)和(0.55±0.23)U/mgprot。随缺氧和冷刺激时间延长,模型组肠组织损伤评分、肠组织中NO、总NOS、诱导型NOS的含量逐渐增加,均高于对照组(P均<0.05),肠组织NO、总NOS、诱导型NOS含量与肠组织损伤程度均呈正相关(r分别为0.865、0.743、0.807,P均<0.05)。结论NO可能是参与肠道屏障损伤过程的重要介质,在NEC肠道屏障损伤发病机制中起重要作用。
Objective To observe the changes of nitric oxide (NO) content, nitric oxide synthase (NOS) activity and intestinal mucosal damage in the pathogenesis of necrotizing enterocolitis (NEC) in neonatal rats. To further elucidate the pathogenesis of NEC, , To find new treatment methods to provide experimental evidence. Methods Thirty newborn SD rats were randomly divided into model group (M) 32 and control group (C) 8. Rats in the model group were fed with milk formula 48h after birth and three times of hypoxia and cold stimulation to establish NEC model. M48, M72, M72, (M96) were sacrificed 8 days after the last hypoxia and cold stimulation respectively. At the end of the experiment, the rats in the control group were sacrificed and the intestines were sacrificed for bowel injury score, NO content and NOS activity in intestinal tissue. Results After modeling, the model group showed diarrhea, abdominal distension, sluggishness and decreased activity. The scores of intestinal injury in M24, M48, M72, M96 and control groups were (1.25 ± 0.56), (1.46 ± 0.31), (2.79 ± 0.40), (3.33 ± 0.59) and (0.08 ± 0.15) (2.07 ± 0.38), (2.88 ± 0.32), (3.09 ± 0.40), (3.98 ± 1.15) and (0.94 ± 0.44) μmol / gprot respectively.The total NOS activity was (2.21 ± 0.42) and (2.77 ± 0.58, 2.95 ± 0.32, 3.80 ± 1.08 and 1.49 ± 0.25 U / mgprot respectively. The inducible NOS activities were (1.25 ± 0.27), (1.94 ± 0.46), (2.06 ± 0.18) and 1.07) and (0.55 ± 0.23) U / mgprot. The scores of NO, total NOS and inducible NOS in intestinal mucosa of model group increased gradually with hypoxia and cold stimulation time (all P <0.05), NO, total NOS , And the level of inducible NOS was positively correlated with the degree of intestinal tissue injury (r = 0.865,0.743,0.807, P <0.05). Conclusion NO may play an important role in the process of intestinal barrier injury and plays an important role in the pathogenesis of intestinal barrier injury in NEC.