机构地区:[1]河北省人民医院消化内科,河北省石家庄市050051
出 处:《世界华人消化杂志》2002年第1期43-47,共5页World Chinese Journal of Digestology
基 金:河北省卫生厅科研基金;No.2K023
摘 要:目的:研究转化生长因子α(TGFα)在慢性胃粘膜病变患者血液、胃液中的含量变化及其与表皮生长因子(EGF)和前列腺素E_2(PGE_2)的关系,初步探讨TGFα在胃粘膜病变发病过程中的作用。 方法:选择经胃镜和病理组织学检查证实的活动期消化性溃疡(PU)患者44例,其中十二指肠球溃疡(DU)22例,胃溃疡(GU)22例;慢性浅表性胃炎(CSG)患者18例;另选择20例胃镜观察胃粘膜基本正常者作为对照组。胃镜下经活检孔抽取胃液,并采集空腹静脉血,用放免分析法检测胃液、血液中TGFα,EGF,PGE_2的含量。 结果:GU和DU两组的血清TGFα(ng·L^(-1)),EGF(ug·L^(-1))含量均明显低于对照组和CSG组(3.5±1.1,3.4±1.3 vs (5.9±1.6.5.0±1.7,p<0.01;0.3±0.1,0.3±0.1 vs 0.6±0.2,0.5±0.2 p<0.01)。GU和DU血浆PGE_2(ng·L^(-1))含量与对照组和CSG组相比,差异无显著性(24.7±8.4,26.0±8.7 vs 25.2±8.0,20.9±7.7,p<0.05).GU,DU和CSG三组胃液中TGFα(ng·L^(-1)),EGF(ng·L^(-1)),PGE_2(ng·L^(-1))含量均明显低于对照组(1.7±0.7,1.6±0.7,2.1±0.7 vs 2.7±0.8,p<0.05;109±47.121±67.113±48 vs 373±78,p<0.01;15.8±6.6, 14.1±7.3,16.4±6.9 vs 21.9±7.5,p<0.05)。GU组胃液中TGFα与PGE_2间存在直线正相关(r=0.55,p<0.05)。AIM: To explore the action of transforming growth factor alpha (TGFa)in gastrointestinal mucosal repair and its relationship with epidermal growth factor ( EGF) and prostaglandin E2 (PGE2).METHODS: Sixty-two patients were selected, including 22 patients with gastric ulcer,22 with duodenal ulcer, 18 with chronic superficial gastritis; and 20 healthy persons were selected as controls. Gastric juice was obtained from all subjects by endoscopy. Venous blood was collected from each subject. The levels of TGFa,EGF and PGE2 in blood and gastric juice were measured by radioimmunoassay.RESULTS: The serum level of TGFa(ng. L1) and EGF(ug. L-1) in patients with gastric ulcer and duodenal ulcer were lower than those in control group and chronic gastritis patients, (3.5±1.1,3.4±1.3 vs 5.9±1.6,5.0± 1.7,P< 0.01; 0.3 ± 0.1,0.3 ± 0.1 vs 0.6±0.2,0.5 ± 0.2 P<0.01). The plasma level of PGE2(ng. L-1 )in patients with gastric ulcer and duodenal ulcer was similar to that in control group and chronic gastritis patients(24.7 ± 8.4,26.0± 8.7 vs 25.2±8.0,20.9±7.7,P>0.05). The gastric juice level of TGFa(ng.L-1) ,EGF(ng. L-1) and PGE2(ng. L-1 )in patients with gastric ulcer, duodenal ulcer and chronic gastritis were all lower than those in control group(1.7±0.7,1.6± 0.7,2.1±0.7 vs 2.7±0.8,P<0.05; 109 ± 47,121 ± 67,113 ±48 vs 373±78, P<0.01; 15.8±6.6,14.1±7.3,16.4±6. 9 vs 21.9±7. 5, P < 0. 05). There was a positive linear correlation between TGFa and PGE2 in gastric juice in patients with gastric ulcer( r = 0.55, P< 0.05). There was no linear correlation between TGFa and EGF, TGFa and PGE2,EGF and PGE2 in blood of patients with gastric ulcer, and in blood and gastric juice of other groups, P>0.05. In gastric ulcer and duodenal ulcer groups, no correlation was found in the TGFa level between blood and gastric juice, P> 0.05. There was no correlation in the PGE2 and EGF levels between blood and gastric juice, P>0.05 in all groups.CONCLUSIONS :Difficiency of TGFa and EGF could lead to ulceration. The protective effect of
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