摘要
目的:检测幽门螺杆菌(H pylori)阳性消化性溃疡(peptic ulcer,PU)患者胃窦黏膜组织学改变和炎症相关基因核因子κB(Nuclear-κB, NF-κB)、人β-防御素-2(human β-denfensin-2, HBD-2)蛋白表达,探讨胃窦黏膜炎症及NF- κB、HBD-2在H pylori相关性PU中的作用及其意义．方法:57例PU患者,其H pylori感染者40例, 非H pylori感染者17例,另设正常对照组8例; 观察各组患者胃窦组织学改变,免疫组化法检测胃窦黏膜NF-κBp65、HBD-2的表达．观察 NF-κBp65、HBD-2的细胞定位情况,用One- Way ANOVA方法比较H pylori感染者与非 H pylori感染者及正常组胃黏膜NF-κBp65、 HBD-2表达量,并对PU不同分期患者胃黏膜 NF-κBp65,HBD-2的表达量进行比较;非参数统计方法分析H pylori感染与PU患者胃窦炎症程度的关系、NF-κBp65、HBD-2表达与胃窦炎症程度的关系及H pylori阳性PU NF- κBp65与HBD-2表达的相关性．结果:PU患者胃窦的炎症程度与H pylori感染程度呈正相关(活动性r=0．374,P<0．01:慢性r=0．333,P<0．05)．在H pylori阳性PU患者 NF-κBp65主要表达于胃黏膜上皮细胞和固有层间质细胞胞核,HBD-2主要表达于胃黏膜表层上皮细胞胞质,二者的表达均较H pylori 阴性组显著增强(6．4±3．28 vs 3．78±2．16, P<0．01;12．96±5．03 vs 4．69±2．05,P<0．01),且均与胃窦黏膜炎症程度具有显著相关性(活动性r=0．744,0．524,P<0．01,慢性r=0．650, 0．606,P<0．01);H pylori阳性PU胃黏膜NF- κBp65表达与HBD-2表达呈正相关关系(r= 0．438,P<0．01)．愈合期和疤痕期PU患者NF- κBp65(4．28±2．11．3．65±2．27)、HBD-2(8．15 ±4．28,6．24±3．71)的表达较活动期者(7．14± 3．24,13．56±5．43)显著降低(P<0．05,P<0．01)．结论:H pylori感染导致胃黏膜NF-κBp65． HBD-2表达增加,胃黏膜炎症程度增强．NF- κB可能通过诱导HBD-2的表达,参与胃窦黏膜炎症反应,从而影响了H Hpylori阳关性PU的病理生理过程．
AIM： To investigate the roles of nuclear factor kappa B （NF-κB）, human β-defensin-2 （HBD-2） and antral gastritis in H pylori-positive peptic ulcer （PU）. METHODS： Patients with H pylori-positive （n = 40） or H pylori-negative （n = 17） PU were included in this study. Eight individual were selected as normal controls. Antral histopathology was observed in the patients and controls.The expression of NF-κBp65 and β-denfensin-2 were measured by immunohistochemistry, and then compared between H pylori-positive and negative patients and normal group as well as between patients with different stages of PU by One-Way ANOVA. Nonparametric statistics was used to analyze the correlations of H pylori infection, NF-κBp65, HBD-2 expression with the degree of antral gastritis. Meanwhile, the relationship between expression of NF-κBp65 and HBD-2 was also analyzed in H pylori-positive PU. RESULTS： The histological severities of both active and chronic inflammation were correlated with H pylori density （active： r= 0.374, P 〈 0.01; chronic： r = 0.333, P 〈 0.05）. NF-κBp65 was expressed mainly in the nucleus of gastric epithelial and mesenchymal cells in lamina propria while HBD-2 was expressed mainly in the cytoplasm of the surface cells of gastric mucosal epithelium. The expression of NF-κBp65 and HBD-2 were significantly higher in H pylori-positive patients than those in H pylori-negative ones （6.4 ± 3.28 vs 3.78 ± 2.16, P 〈 0.01; 12.96 ± 5.03 vs 4.69 ± 2.05, P 〈 0.01）, and both expression of NF-κBp65 and HBD-2 were correlated with histological severity of active and chronic inflammation （active： r = 0.744, 0.524, P 〈 0.01; chronic： r = 0.650, 0.606, P 〈 0.01）. There was a positive correlation between the expression of NF-κBp65 and HBD-2 （r = 0.438, P 〈 0.01）. The expression of NF-κBp65 （4.28 ± 2.11, 3.65 ± 2.27） and HBD-2 （8.15 ± 4.28, 6.24 ± 3.71） in PU patients at the stage of healing and scaring were lower significantly than those （7.14 ± 3.24, 13.56 ± 5.43） of PU patients at active stage （P 〈 0.05 or P 〈 0.01）. CONCLUSION： H pylori infection leads to the over-expression of NF-κB and HBD-2 and enhancement of active and chronic inflammation. NF-κB activation may contribute to the induction of HBD-2 expression, and play an important role in the pathogenesis of H pylori-positive PU.
出处
《世界华人消化杂志》
CAS
北大核心
2006年第4期376-381,共6页
World Chinese Journal of Digestology
基金
湖南省科技计划重点项目
No.02SSY1005-4
