姜黄素对新生大鼠坏死性小肠结肠炎的保护作用

Protective effects of curcumin on neonatal rats with necrotizing enterocolitis

摘要:

目的：通过研究姜黄素对新生大鼠坏死性小肠结肠炎(NEC)肠组织病理改变，环氧合酶-2(COX-2)表达，肿瘤坏死因子α(TNF-α)及白细胞介素-10 (IL-10)生成的影响，探讨姜黄素对NEC是否有保护作用。方法：40只新生大鼠随机分为4组：正常对照组，溶剂对照组，NEC模型组,姜黄素干预组，每组10只。每日定时观察各组大鼠的一般情况，连续3 d并于第4天处死，取肠道组织检测病理改变，TNF-α、IL-10含量及COX-2的表达。结果：姜黄素能改善NEC模型大鼠一般情况及病理组织学征象；与正常对照组、溶剂对照组比较，NEC模型组,姜黄素干预组TNF-α、IL-10浓度显著增高(P<0.05)；姜黄素干预组TNF-α浓度较NEC模型组显著下降(P<0.05)、IL-10浓度较NEC模型组显著升高(P<0.05)；姜黄素干预组COX-2表达量显著低于NEC模型组。结论：姜黄素对NEC大鼠具有保护作用，其机制可能与姜黄素抑制COX-2的表达，减少TNF-α的含量、增加 IL-10的含量有关。［中国当代儿科杂志，2010，12（2）：132-136］

Abstract:

OBJECTIVE: This study examined the effects of curcumin on intestinal histopathological changes, cyclooxygenase-2 (COX-2) expression, and tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) concentrations in neonatal rats with necrotizing enterocolitis (NEC) , in order to investigate the effects of curcumin against NEC. METHODS: Forty neonatal rats were randomly divided into four groups (n=10 each): normal control, solvent control, NEC model, and curcumin intervention. The general situations of rats were observed for 3 consecutive days, and the rats were then sacrificed on the 4th day. Intestinal tissues were obtained for examining the histopathological changes, COX-2 expression, and TNF-α and IL-10 concentrations. RESULTS: Curcumin treatment ameliorated the general situations and histopathological signs in rats with NEC. TNF-α and IL-10 concentrations in the NEC model and the curcumin intervention groups increased significantly compared with those in the normal and solvent control groups (P<0.05). The concentration of TNF-α decreased (P<0.05), while the concentration of IL-10 increased significantly in the curcumin intervention group in comparison with the NEC model group (P<0.05). Immunohistochemistry results indicated that the positive expression of COX-2 in the curcumin intervention group was significantly lower than that in the NEC model group. CONCLUSIONS: Curcumin has protective effects against NEC in neonatal rats, possibly through inhibiting COX-2 expression, reducing TNF-α content, and increasing IL-10 content.［Chin J Contemp Pediatr, 2010, 12 (2):132-136］