摘要
目的 探讨环氧化物酶2(COX2)及其产物前列腺素I_2(PGI_2)在门静脉高压性胃病(PHG)发病中的作用。方法 40只Wistar大鼠,随机分为手术组(32只)和对照组(8只)。手术组以门静脉部分结扎复制大鼠PHG模型,分别在手术后1、2、3、4周(每周8只大鼠)测自由门静脉压力;并处死动物,肉眼和光镜观察大鼠胃黏膜病变情况;用放射免疫法测定门静脉血及胃黏膜匀浆中PGI_2的稳定代谢产物6-酮-前列腺素F1α含量;用免疫组织化学染色观察各期胃组织中COX2的表达情况。结果 门静脉结扎后其压力很快升高,术后1、2、3、4周分别为(2.40±0.15)kPa、(2.38±0.17)kPa、(2.52±0.21)kPa和(2.46±0.17)kPa,与对照组(0.90±0.16)kPa比较,t值分别为19.345、17.931、17.356、18.900,P<0.05;肉眼观察见胃黏膜苍白水肿、充血、浅表糜烂及点状出血,并随门静脉结扎时间的延长而日益加重;光镜下见胃黏膜层及黏膜下层增厚,血管扩张,血管断面增加,血管周围有淋巴细胞及中性粒细胞浸润;术后1周门静脉血及胃黏膜中6-酮-前列腺素F1α含量很快升高分别为(104.52±25.11)pg/ml和(180.21±37.56)pg/ml并维持在较高水平,明显高于对照组[分别为(73.62±20.33)pg/ml和(142.11±31.51)pg/ml],t值为2.710和2.198,P<0.05。免疫组织化学染色结果显示第1、2、3、
Objective To study the role of cyclooxygenase 2 (COX 2) and prostaglandin I2 (PGI2) in the development of portal hypertensive gastropathy (PHG). Methods Forty Wistar rats were divided into surgery group (32) and control group (8). Partial portal vein ligation method was used to narrow the sectional area of portal vein to establish the experimental model of PHG in surgery group rats. Then they were divided into four groups (8 rats in each). The free pressure of portal vein was determined at the 1st, 2nd, 3rd, 4th weeks after the operation, and 8 rats were killed to observe the pathological change of gastric mucosa. The levels of 6-keto-PGFl alpha, a stable metabolite of PGI2, were determined by radioimmunoassay in gastric mucosa homogenate and the blood of portal vein. The expression of COX 2 in gastric mucosa was determined by immunohistochemistry. Results The free pressure of portal vein increased rapidly after partial portal vein ligation and maintained a high stable level after 1 week. They were (2.40±0.15) kPa, (2.38±0.17) kPa, (2.52±0.21) kPa, and (2.46±0.17) kPa at the 1st, 2nd, 3rd, and 4th weeks after partial portal vein ligation, while it was (0.90±0.16) kPa in control group (t≥17.356, P < 0.05). The gastric mucosa appeared pale, edema, hyperaemia, surface erosion, punctate hemorrhage and these lesions were more apparent with the time after the operation. The pathological examination showed that the gastric mucosa and submucosa thickened. The vessels of gastric mucosa and submucosa expanded and increased. There were lymphocytes and neutrophils infiltration around the vessels in the gastric mucosa and submucosa. The 6-keto-PGFl alpha levels in gastric mucosa and the blood of portal vein increased rapidly and maintained a high level after partial portal vein ligation,which were higher than those in control group (104.52 pg/ml++++++++ 25.11 pg/ml vs 73.62 pg/ml ±20.33 pg/ml, t = 2.710, P < 0.05; 180.21 pg /ml ±37.56 pg /ml vs 142.11 pg /ml±31.51 pg /ml, f = 2.198, P < 0.05). The results of immunohistochemistry showed that the intensity and degree of the COX 2 staining in gastric tissue increased at the 1st, 2nd, 3rd, 4th weeks after partial portal vein ligation, while the COX 2 in control group rats was negative. Conclusions The expression of COX 2 and PGI2 in gastric tissue increased in portal hypertension. PGI2 as an inflammatory medium, damages the gastric mucosa by expanding vessels and other mechanisms in portal hypertension. It may be one of the important factors contributing to the development of PHG.
出处
《中华肝脏病杂志》
CAS
CSCD
2003年第9期536-538,共3页
Chinese Journal of Hepatology
