通过观察罹患坏死性小肠结肠炎(necrotizing enterocolitis，NEC)的新生SD大鼠肠组织中分泌型磷脂酶A₂(secretory phospholipase A₂，sPLA₂)含量变化，探讨分泌型磷脂酶A₂在坏死性小肠结肠炎发病中的作用。

将20只新生SD大鼠随机分成NEC模型组(n＝10)和对照组(n＝10)。对NEC模型组新生SD大鼠自出生48 h后给予鼠乳代用品人工喂养，并对其进行100%氮气缺氧90 s和4℃冷刺激10 min处理，每天2次，连续处理3 d，建立新生SD大鼠坏死性小肠结肠炎模型。在最后一次缺氧、冷刺激处理后24 h，将其空腹断头处死，同时处死对照组SD大鼠。对两组新生SD大鼠均留取回盲部近端肠管组织标本，分别进行肠组织损伤评分和肠组织分泌型磷脂酶A₂含量检测。当标本组织学评分≥2分时，诊断为坏死性小肠结肠炎。采用酶联免疫吸附测定(enzyme linked immunosorbent assay，ELISA)法检测肠组织中分泌型磷脂酶A₂含量(单位为：pg/mg prot)。应用Kruskal-Wallis H检验等方法对两组大鼠肠组织中分泌型磷脂酶A₂含量进行统计学分析(α＝0.05)。

NEC模型组新生SD大鼠相继出现腹泻、腹胀、萎靡、活动减少，生长减慢等症状；对照组新生SD大鼠进食及排便正常，无腹泻及腹胀症状，活动度良好，皮下脂肪丰满。NEC模型组和对照组肠组织损伤病理学评分(±s)分别为：3.300±0.850和0.450±0.400；肠组织分泌型磷脂酶A₂含量(pg/mg prot)分别为1.752±0.483和0.669 ±0.180。两组间肠组织损伤评分和肠组织中分泌型磷脂酶A₂含量比较，差异均有显著意义(P<0.05)；肠组织分泌型磷脂酶A₂含量与相应平均损伤程度，均呈显著正相关关系(rsPLA₂＝0.834，P＝0.000)。NEC模型组新生SD大鼠坏死性小肠结肠炎发生率为100%(10/10)，对照组无一例发生坏死性小肠结肠炎。

肠组织分泌型磷脂酶A₂是导致坏死性小肠结肠炎发生的关键介质，持续过度表达分泌型磷脂酶A₂介导，可致黏膜损伤和肠屏障功能障碍，从而引发坏死性小肠结肠炎。

To study the content change of phospholipase A₂ (sPLA₂) in neonatal SD rat model of necrotizing enterocolitis, and analyze the correlation between the secretory phospholipase A₂ level and the scoring of intestinal injury.

Twenty neonatal SD rats [48 hours olds, weighing (5~10)g] were divided into NEC model group (n=10) and control group (n=10). NEC model group was made into necrotizing enterocolitis models as follows: Separate from mother rats and feeding with rat milk substitute, hypoxia(100% N₂) for 90 second and 4℃ cold exposure for 10 minutes, twice a day during 3 consecutive days. Control group was given rat milk feeding, not hypoxia and cold exposure. On the fourth day all the subjects were sacrificed and the intestine around ileocecal junction were obtained to evaluated by stained with H&E for histological analysis and score. The mean scores more than 2 were considered as necrotizing enterocolitis. The contents of secretory phospholipase A₂ in homogenate of intestinal tissue were measured by enzyme linked immunosorbent assay(ELISA), and were expressed pg per mg protein of intestinal tissue. Kruskal-Wallis H test and Spearman correlation analysis were used to analyze difference among various groups.

Neonatal rats in NEC model group had diarrhea, abdominal distention, growth and development stepping down, activity reducing, and neonatal rats in control group was healthy. The scores of histological evaluation (±s) in NEC model group and control group were 3.300±0.850, 0.450±0.400, and contents of secretory phospholipase A₂ in intestinal tissue were 1.752±0.483, 0.669±0.180, respectively. The score of histopathology and the content of secretory phospholipase A₂ in intestinal tissue had significant difference between two groups. By Spearman correlation analysis, the relations of the degree of intestinal injury and the contents of secretory phospholipase A₂ in intestinal tissue was positive(r_sPLA2=0.834, P<0.05).

Endogenous secretory phospholipase A₂ in intestine tissue are probably the critical factors for the development of necrotizing enterocolitis. Continued over-expression of secretory phospholipase A₂ will mediate injury of intestinal mucosal and the dysfunction of intestinal barrier, thereby triggering necrotizing enterocolitis.