预防性应用天然蒙脱石对新生大鼠坏死性小肠结肠炎肠损伤的保护作用及机制探讨
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摘要
目的探讨预防性应用天然蒙脱石对新生鼠坏死性小肠结肠炎(NEC)模型肠损伤保护作用及可能机制,为预防性应用天然蒙脱石防治NEC提供科学依据。
方法SD新生鼠出生后48小时开始给予鼠配方奶喂养,100%氮气缺氧90秒,4℃冷刺激10分钟,每天2次,连续3天建立新生鼠NEC模型。按析因设计,32只新生SD大鼠随机分成4组,每组动物各8只。A组为NEC模型组并在出生48小时起每日给予天然蒙脱石灌胃(0.6g/kg/d);B组为NEC模型组,未添加天然蒙脱石;C组为对照组,未添加天然蒙脱石;D组为对照组并给予天然蒙脱石(0.6g/kg/d);在最后一次缺氧、冷刺激后24小时空腹断头处死大鼠,留取十二指肠下端至直肠上端肠管进行肠细胞凋亡率检测及电镜观察。再选取32只新生SD大鼠,按上述分组和实验方法,同期留取十二指肠下端至直肠上端肠管检测PAF、TNF-α含量。所有新生鼠均留取回盲部近端肠管进行肠组织损伤评分。采用流式细胞仪检测肠细胞凋亡率,ELISA法检测肠组织PAF、TNF-α含量(pg/mg prot)。采用SPSS11.0统计学软件进行统计分析,α=0.05为显著性检验标准。
结果[1]开始造模后,A、B组新生SD大鼠相继出现腹泻、腹胀、萎靡、活动减少,生长减慢;透射电镜显示肠黏膜出现大量凋亡细胞,有些形成凋亡小体,A组程度较轻。A、B、C和D组肠组织损伤评分(?x±s )分别为1.42±0.36、3.54±0.50、0.13±0.17和0.17±0.18;肠细胞凋亡率(%)分别为11.6±4.6、27.6±9.9、4.8±2.9和3.6±3.8。各组之间肠组织损伤评分、肠组织细胞凋亡率差别有显著意义;与B组相比,A组肠组织损伤评分和肠组织细胞凋亡率明显降低,但仍高于C、D两组,差异均有显著意义。[2]A、B、C和D组肠组织PAF含量(?x±s )分别为385.0±308.0、1663.2±576.1、40.8±40.4和37.1±33.1;TNF-α含量为46.4±15.1、258.1±281.7、13.2±12.2和12.4±8.8。各组之间肠组织PAF、TNF-α含量差别均有显著意义;B组肠组织PAF、TNF-α含量明显高于C、D组;与B组相比,A组肠组织PAF、TNF-α含量明显降低;差异均有统计学意义。[3]析因设计方差分析显示:肠组织损伤评分、肠组织细胞凋亡率及肠组织PAF、TNF-α含量均受造模和预防性应用天然蒙脱石两因素影响,造模与预防性应用天然蒙脱石之间存在交互作用;新生大鼠肠损伤程度与肠组织细胞凋亡率、肠组织PAF、TNF-a含量呈显著正相关(r凋亡率=0.853,rPAF=0.852,rTNF-α=0.839,p均<0.01)。
结论预防性应用天然蒙脱石可以降低新生NEC大鼠肠损伤程度,可能通过减少其肠细胞凋亡率,降低肠组织PAF、TNF-α含量,下调对机体有害的炎症级联反应,从而减轻肠损伤,降低新生大鼠发生NEC危险性。
Objective To explore the protective effects and the mechanism of smectite powder in inhibit intestinal injury of neonatal Sprague-Dewley rat necrotizing enterocolitis(NEC) model.
Methods According to 2×2 factor analysis, 32 neonate Sprague-Dewley rats(48 hours olds, weighing 5～10g) were divided into 4 groups(A, B, C and D, n=8 rats each groups). Rats in Group A and B were made into NEC 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. Rats in group A was given smectite powder(0.6g/kg/d) and rats in group B was not. Rats in groups C and D served as control groups, as well as rats in group D was given smectite powder(0.6g/kg/d) and those in group C was not. On the 4th day the rats were sacrificed and intestinal tissue were collected. The apoptosis ratio of intestinal cells were determined with flow cytometry(FCM) and the morphological changes in intestinal musca were observed under light and electron microscope. Another 32 neonate Sprague-Dewley rats were divided into 4 groups also, and the empirical methods were same as described above. The intestinal tissue were obtained to measure the content of PAF, TNF-αwith ELISA(pg/mg prot). The intestine around ileocecal junction of all the subjects were scored in double-blind way, and the mean score more than 2 were considered NEC. Kruskal-Wallis H test, factorial ANOVA were used to analyze difference among various groups.α=0.05 was considered significant.
Result [1]After separate from mother rats, feeding with rat milk substitute and induced by hypoxia and cold exposure several continual times, neonatal rats in Groups A and B had diarrhea, abdominal distention, growth and development stepping down, activity reducing, and the apoptosis cells and apoptic body in intestine mucosa was observed in some degree. As compared with group B, there were remarkably relieved after given smectite powder in group A. The scores of histological evaluation(?x±s ) in group A, B, C and D were 1.42±0.36, 3.54±0.50, 0.13±0.17 and 0.17±0.18, and the apoptosis ratio of intestinal cells were 11.6±4.6, 27.6±9.9, 4.8±2.9 and 3.6±3.8, respectively. The score of histopatholigical and the apoptosis ratio of intestinal cells had significant difference among groups. Comparing with that of group B, the score of histopatholigical and the apoptosis ratio of intestinal cells of group A reduced, but that of group A was higher than two control groups significantly. [3]In Group A, B, C and D, the content of PAF(?x±s, pg/mg prot ) in intestinal tissue were 385.0±308.0, 1663.2±576.1, 40.8±40.4 and 37.1±33.1, and the TNF-αwere 46.4±15.1, 258.1±281.7, 13.2±12.2 and 12.4±8.8, respectively. There were significant difference about PAF, TNF-αamong groups. Comparing with those in group B, the contents of PAF, TNF-αin group A reduced significantly, but they were higher thangroup C and D, and differences were significant. [3]By factorial ANOVA, two factors of model and smectite powder intervention had taken effect on the score of histopatholigical, the apoptosis ratio of intestinal cells and the contents of PAF, TNF-α. There were interaction between model and smectite powder intervention. By spearman correlation analysis, the relation of the apoptosis ratio of intestinal cells, the contents of PAF, TNF-αin intestinal tissue and the degree of intestinal injury were positive(rapoptosis ratio=0.853, rPAF=0.852, rTNF-α=0.839, p<0.01).
Conclusion Smectite powder is beneficial to reduce the intestinal injury of neonate rats caused by formula feeding, hypoxia and cold exposure and decrease the incidence of NEC of neonate rats. It may reduced the apoptosis ratio of intestinal cells and decrease the endogenous production of PAF and TNF-αin intestinal tissue, which would be underlying protective mechanisms of smectite powder on NEC.
方法SD新生鼠出生后48小时开始给予鼠配方奶喂养,100%氮气缺氧90秒,4℃冷刺激10分钟,每天2次,连续3天建立新生鼠NEC模型。按析因设计,32只新生SD大鼠随机分成4组,每组动物各8只。A组为NEC模型组并在出生48小时起每日给予天然蒙脱石灌胃(0.6g/kg/d);B组为NEC模型组,未添加天然蒙脱石;C组为对照组,未添加天然蒙脱石;D组为对照组并给予天然蒙脱石(0.6g/kg/d);在最后一次缺氧、冷刺激后24小时空腹断头处死大鼠,留取十二指肠下端至直肠上端肠管进行肠细胞凋亡率检测及电镜观察。再选取32只新生SD大鼠,按上述分组和实验方法,同期留取十二指肠下端至直肠上端肠管检测PAF、TNF-α含量。所有新生鼠均留取回盲部近端肠管进行肠组织损伤评分。采用流式细胞仪检测肠细胞凋亡率,ELISA法检测肠组织PAF、TNF-α含量(pg/mg prot)。采用SPSS11.0统计学软件进行统计分析,α=0.05为显著性检验标准。
结果[1]开始造模后,A、B组新生SD大鼠相继出现腹泻、腹胀、萎靡、活动减少,生长减慢;透射电镜显示肠黏膜出现大量凋亡细胞,有些形成凋亡小体,A组程度较轻。A、B、C和D组肠组织损伤评分(?x±s )分别为1.42±0.36、3.54±0.50、0.13±0.17和0.17±0.18;肠细胞凋亡率(%)分别为11.6±4.6、27.6±9.9、4.8±2.9和3.6±3.8。各组之间肠组织损伤评分、肠组织细胞凋亡率差别有显著意义;与B组相比,A组肠组织损伤评分和肠组织细胞凋亡率明显降低,但仍高于C、D两组,差异均有显著意义。[2]A、B、C和D组肠组织PAF含量(?x±s )分别为385.0±308.0、1663.2±576.1、40.8±40.4和37.1±33.1;TNF-α含量为46.4±15.1、258.1±281.7、13.2±12.2和12.4±8.8。各组之间肠组织PAF、TNF-α含量差别均有显著意义;B组肠组织PAF、TNF-α含量明显高于C、D组;与B组相比,A组肠组织PAF、TNF-α含量明显降低;差异均有统计学意义。[3]析因设计方差分析显示:肠组织损伤评分、肠组织细胞凋亡率及肠组织PAF、TNF-α含量均受造模和预防性应用天然蒙脱石两因素影响,造模与预防性应用天然蒙脱石之间存在交互作用;新生大鼠肠损伤程度与肠组织细胞凋亡率、肠组织PAF、TNF-a含量呈显著正相关(r凋亡率=0.853,rPAF=0.852,rTNF-α=0.839,p均<0.01)。
结论预防性应用天然蒙脱石可以降低新生NEC大鼠肠损伤程度,可能通过减少其肠细胞凋亡率,降低肠组织PAF、TNF-α含量,下调对机体有害的炎症级联反应,从而减轻肠损伤,降低新生大鼠发生NEC危险性。
Objective To explore the protective effects and the mechanism of smectite powder in inhibit intestinal injury of neonatal Sprague-Dewley rat necrotizing enterocolitis(NEC) model.
Methods According to 2×2 factor analysis, 32 neonate Sprague-Dewley rats(48 hours olds, weighing 5～10g) were divided into 4 groups(A, B, C and D, n=8 rats each groups). Rats in Group A and B were made into NEC 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. Rats in group A was given smectite powder(0.6g/kg/d) and rats in group B was not. Rats in groups C and D served as control groups, as well as rats in group D was given smectite powder(0.6g/kg/d) and those in group C was not. On the 4th day the rats were sacrificed and intestinal tissue were collected. The apoptosis ratio of intestinal cells were determined with flow cytometry(FCM) and the morphological changes in intestinal musca were observed under light and electron microscope. Another 32 neonate Sprague-Dewley rats were divided into 4 groups also, and the empirical methods were same as described above. The intestinal tissue were obtained to measure the content of PAF, TNF-αwith ELISA(pg/mg prot). The intestine around ileocecal junction of all the subjects were scored in double-blind way, and the mean score more than 2 were considered NEC. Kruskal-Wallis H test, factorial ANOVA were used to analyze difference among various groups.α=0.05 was considered significant.
Result [1]After separate from mother rats, feeding with rat milk substitute and induced by hypoxia and cold exposure several continual times, neonatal rats in Groups A and B had diarrhea, abdominal distention, growth and development stepping down, activity reducing, and the apoptosis cells and apoptic body in intestine mucosa was observed in some degree. As compared with group B, there were remarkably relieved after given smectite powder in group A. The scores of histological evaluation(?x±s ) in group A, B, C and D were 1.42±0.36, 3.54±0.50, 0.13±0.17 and 0.17±0.18, and the apoptosis ratio of intestinal cells were 11.6±4.6, 27.6±9.9, 4.8±2.9 and 3.6±3.8, respectively. The score of histopatholigical and the apoptosis ratio of intestinal cells had significant difference among groups. Comparing with that of group B, the score of histopatholigical and the apoptosis ratio of intestinal cells of group A reduced, but that of group A was higher than two control groups significantly. [3]In Group A, B, C and D, the content of PAF(?x±s, pg/mg prot ) in intestinal tissue were 385.0±308.0, 1663.2±576.1, 40.8±40.4 and 37.1±33.1, and the TNF-αwere 46.4±15.1, 258.1±281.7, 13.2±12.2 and 12.4±8.8, respectively. There were significant difference about PAF, TNF-αamong groups. Comparing with those in group B, the contents of PAF, TNF-αin group A reduced significantly, but they were higher thangroup C and D, and differences were significant. [3]By factorial ANOVA, two factors of model and smectite powder intervention had taken effect on the score of histopatholigical, the apoptosis ratio of intestinal cells and the contents of PAF, TNF-α. There were interaction between model and smectite powder intervention. By spearman correlation analysis, the relation of the apoptosis ratio of intestinal cells, the contents of PAF, TNF-αin intestinal tissue and the degree of intestinal injury were positive(rapoptosis ratio=0.853, rPAF=0.852, rTNF-α=0.839, p<0.01).
Conclusion Smectite powder is beneficial to reduce the intestinal injury of neonate rats caused by formula feeding, hypoxia and cold exposure and decrease the incidence of NEC of neonate rats. It may reduced the apoptosis ratio of intestinal cells and decrease the endogenous production of PAF and TNF-αin intestinal tissue, which would be underlying protective mechanisms of smectite powder on NEC.
引文
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[1]Treszl A, Tulassay T, Vasarhelyi B. Genetic basis for necrotizing enterocolitis-risk factors and their relations to genetic polymorphisms[J]. Front Biosci, 2006, 11: 570-580.
[2]Bober-Olesinska K, Kornacka MK. Effects of glutamine supplemented parenteral nutrition on the incidence of necrotizing enterocolitis, nosocomial sepsis and length of hospital stay in very low birth weight infants[J]. Med Wieku Rozwoj, 2005, 9(3 Pt 1): 325-333.
[3]黄瑛, 邵肖梅, Josef Neu. 免疫营养素和新生儿感染[J]. 国外医学儿科学分册, 2003, 30(3): 113.
[4]Dvorak B, Fituch CC, Williams CS, et al. Increased epidermal growth factor levels in humam milk of mothers with extremely premature infants.pediatr Res 2003; 54: 15-19.
[5]Shin CE, Falcone RA Jr, Stuart L. Diminished epidermal growth factor levels in infants with necrotizing enterocolitis[J]. Pediatr Surg,2000,35(2):173～176.
[6]毛志芹, 孟庆学, 孙梅, 等. 窒息后新生儿血中表皮生长因子、神经降压素及生长抑素水平的研究及与临床因素关系的探讨[J]. 新生儿科杂志, 2002, 17(5): 193-195.
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[1]Treszl A, Tulassay T, Vasarhelyi B. Genetic basis for necrotizing enterocolitis-risk factors and their relations to genetic polymorphisms[J]. Front Biosci, 2006, 11: 570-580.
[2]Bober-Olesinska K, Kornacka MK. Effects of glutamine supplemented parenteral nutrition on the incidence of necrotizing enterocolitis, nosocomial sepsis and length of hospital stay in very low birth weight infants[J]. Med Wieku Rozwoj, 2005, 9(3 Pt 1): 325-333.
[3]黄瑛, 邵肖梅, Josef Neu. 免疫营养素和新生儿感染[J]. 国外医学儿科学分册, 2003, 30(3): 113.
[4]Dvorak B, Fituch CC, Williams CS, et al. Increased epidermal growth factor levels in humam milk of mothers with extremely premature infants.pediatr Res 2003; 54: 15-19.
[5]Shin CE, Falcone RA Jr, Stuart L. Diminished epidermal growth factor levels in infants with necrotizing enterocolitis[J]. Pediatr Surg,2000,35(2):173～176.
[6]毛志芹, 孟庆学, 孙梅, 等. 窒息后新生儿血中表皮生长因子、神经降压素及生长抑素水平的研究及与临床因素关系的探讨[J]. 新生儿科杂志, 2002, 17(5): 193-195.
[7]Dvorak B, Halpern MD, Holubec H,etal. Epidermal growth factor reduces the development of necrotizing enterocolitis in a neonatal rat model[J]. Am J Physiol,2002,282(1):G156~G164.
[8]Chiou SK, Tanigawa T, Akahoshi T, etal. Survivin:a novel target for indomethacin-induced gastric injury. Gastroenterology 2005: 128: 63-73.
[9]刘春英, 王丽杰, 孙梅, 等. 在 PGE2 在内毒素诱导的幼鼠急性胃黏膜损伤中的变化及PAF 受体拮抗剂对其影响. 世界华人消化杂志, 2006; 14(2): 163-166.
[10]Mammen JMV, Matthews JB. Mucosal repair in the gastrointestinal tract. Crit Care Med 2003; 31: S532-S537.
[11]Renes IB, Verburg M, Van Nispen DJ, etal. experimental colitis: alterations in carbonic anhydrase I, mucin MUC2, and trefoil factor 3 expression. Int J Colorectal Dis 2002; 17: 317-326.
[12]Emami S, Le Floch N, Bruyneel E, etal. Induction of scattering and cellular invasion bytrefoil peptides in sac and RhoAtransformed kidney and colonic epithelial cells[J]. FASEB J , 2001, 15(2): 351-361.
[13]Marchbank T, Cox HM, Goodlad RA, etal. Effect of ectopic expression of rat trefoil factor family 3 (intestinal trefoil factor) in the jejunum of transgenic mice. J Biol Chem. 2001; 76: 24088-24096.
[14]Zhang BH, Yu HG, Sheng ZX, etal. The therapeutic effect of recombinant human trefoil factor 3 on hypoxia-induced necrotizing enterocolitis in immature rat. Regul Pept 2003; 116: 53-60.
[15]Renes IB, Verburg M, Van Nispen DJ, etal. Distinct epithelial responses in experimental colitis: implications for ion uptake and mucosal protection. Am J Physiol Gastrointest liver Physiol2002; 283: G169-G179.
[16]李军, 赵亚娟, 孙梅, 等. 肠三叶因子对内毒素诱导幼鼠肠组织 NO 和 MDA 的作用.世界华人消化杂志, 2006; 14(1): 63-67.
[17]Giraud AS, Pereira PM, Thim L, etal. TFF-2 inhibits iNOS/NO in monocytes and nitrated protein in healing colon after colitis. Peptides 2004; 25: 803-809.
[18]Lin J, Nadroo AM, Chen W, etal. Ontogeny and prenatal expression of trefoil factor 3/ITF in the human intestine. Early Hum Dev 2003, 71: 103-109.
[19]Lin J, Holzman IR, Jiang P, etal. Expression of intestinal trefoil factor in developing rat intestine[J]. Biol Neonate,1999,76(2):92~97.
[20]许玲芬, 王丽杰, 孙梅, 等. 肠三叶因子在宫内窒息鼠肠道内表达的研究. 中国优生与遗传杂志, 2005; 13(11)66-68.
[21]陈丽萍, 张丙宏, 李艳, 等. 肠三叶因子对新生鼠缺氧肠损伤模型白细胞介素 8、丙二醛的影响及其意义. 中华围产医学杂志, 2003, 6(5): 306-309.
[22]Han X, Fink MP, Delude RL. Proinflammatory cytokines cause NO-dependent and- independent changes in expression and localization of tight junction proteins in intestinal epithelial cells. Shock2003; 19: 229-237.
[23]Di Lorenzo M, Krantis A. Nitric oxide synthase isoenzyme activities in a premature piglet model of necrotizing enterocolitis: effects of nitrergic manipulation. Pediatr Surg Int. 2002; 18: 624-629.
[24]Morin MJ, Karr SM, Faris RA, etal. Developmental variability in expression and regulationof inducible nitric oxide synthase in rat intestine. Am J Physiol Gastrointest Liver Physiol 2001; 281: G552-G559.
[25]Potoka DA, Nadler EP, Upperman JS, etal. Role of nitric oxide and peroxynitrite in gut barrier failure. World J Surg 2002; 26: 806-811.
[26]Forsythe RM, Xu DZ, Lu Q, etal. Lipopolysaccharide-induced enterocyte-derived nitric oxide induces intestinal monolayer permeability in an autocrine fashion. Shock 2002; 17: 180-184.
[27]Chen LW, Hsu CM, Huang JK, etal. Effects of bombesin on gutmucosal immunity in rats after thermal injury[ J ]. J FormosMed Assoc, 2000, 99(6): 491-498.
[28]Wang ZT, Yao YM, Xiao GX, etal. Risk factors of development of gut-derived bacterial translocation in thermally injured rats[J]. World J Gastroenterol, 2004, 10(11): 1619-1624.
[29]Bollinger RR, EverettML, Palestrant D, etal. Human secretory immunoglobulin A may contribute to biofilm formation in the gut[J]. Immunology, 2003, 109(4): 580-587.
[30]Ikeda S, Zarzaur BL, Johnson CD, etal. Total parenteral nutrition supplementation with glutamine improves survival after gut ischemia/ reperfusion[J]. JPEN J Parenter Enteral Nutr, 2002, 26(3): 169-173.
[31]Rey J, Garin N, Spertini F, etal. Targeting of secretory IgA to Peyer's patch dendritic and T cells after transport by intestinal M cells. [J]Immumol, 2004; 172: 3026-3033.
[32]Phalipon A, Cardona A, Kraehenbuhl JP, etal. Secretory component: a new role in secretory IgA-mediated immune exclusion in vivo. Immunity, 2002; 17: 107-115.
[33]Royle L, Roos A, Harvey DJ, etal. Secretory IgA N- and O-glycans provide a link between the innate and adaptive immune systems. [J]Biol Chem, 2003; 278: 20140-20153.
[34]Kalia N, Bardhan KD, Reed MW, etal. Mechanisms of Helicobacter pylori -induced rat gastric mucosal microcirculatory disturbances in vivo[J]. Dig Dis Sci, 2000, 45(4): 763-772.
[35]Ewer AK, Al-Salti W, Coney AM, etal. The role of platelet activating factor in a neonatal piglet model of necrotising enterocolitis[J]. Gut, 2004, 53(2): 207-213.
[36]Liu Q, Djuricin G, Rossi H, etal. The effect of lexipafant on bacterial translocation in acute necrotizing pancreatitis in rats[J]. Am Surg, 1999, 65(7): 611-616.
[37]Yeh KY, Yeh M, Glass J, et al. Rapid activation of NF-kappaB and AP-1 and target gene expression in postischemic rat intestine. Gastroenterology, 2000, 118(3): 525-534.
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