摘要
目的 :探讨细胞凋亡与细胞因子在胃溃疡愈合中的意义。方法 :应用原位末端标记法和免疫组织化学法观察胃溃疡治疗前后胃黏膜细胞凋亡 ,表皮生长因子受体 (EGFR)、细胞外信号调节激酶 (ERK 1)和 SMAD3表达的变化。结果 :2 0例胃溃疡患者抗溃疡治疗后幽门螺杆菌 (Hp)根除率为 6 6 .6 % ,溃疡全部愈合 ,平均细胞凋亡指数由治疗前的 2 1.3%下降至治疗后的5 .6 % ,OR=0 .0 31,95 % CI=0 .0 0 5～ 0 .177,治疗前后的 EGFR分级无显著差异 (P>0 .0 5 ) ;SMAD3的吸光值由治疗前的0 .912± 0 .0 15下降至治疗后的 0 .35 2± 0 .0 31,OR=0 .0 14 ,95 % CI=0 .0 0 1～ 0 .132 ;活动期溃疡 ERK1的吸光值为 0 .86 1±0 .0 38,OR=39,95 % CI=4 .177～ 36 4 .137,治疗后的吸光值明显降低 (0 .347± 0 .0 2 6 ,P <0 .0 1)。结论 :Hp诱导细胞凋亡参与胃溃疡的形成并影响愈合 ,细胞因子 EGFR、SMAD3和 ERK1可能通过调节细胞凋亡而影响胃溃疡的形成和愈合过程。
Objective:To investigate effects of apoptosis and cytokines on gastric ulcer healing.Methods:Apoptosis was detected by TUNEL and Epidermal growth factor receptor(EGFR), SMAD3 and extracellular signal-regulated kinase(ERK1) by immunohistochemical staining before and after anti-ulcer treatment in patients with gastric ulcer.Result:After anti-ulcer treatment, eradication rate of helicobacter pylori(Hp) was 66.6%. Gastric ulcer was healed in all patients and mean apoptosis index was decreased from 21.3% to 5.6%(OR=0.031, 95%CI=0.005～0.177). There was no significant difference in EGFR expressions before and after anti-ulcer treatment(P>0.05). After anti-ulcer treatment, expression of SMAD3 was significantly lower than that before treatment(0.352±0.031 vs. 0.912±0.015, OR=0.014, 95%CI=0.001～0.132). ERK1 was in high expression in active gastric ulcer(0.861±0.038,OR=39, 95%CI=4.177～364.137) and in low expression after anti-ulcer treatment(0.347±0.026,P<0.01).Conclusion:Apoptosis induced by Hp affects the development and healing of gastric ulcer. EGFR, ERK1 and SMAD3 may regulate apoptosis and then take effect on the development and healing of gastric ulcer.
出处
《广西医科大学学报》
CAS
北大核心
2005年第1期23-26,共4页
Journal of Guangxi Medical University
基金
广西自然科学基金资助项目 (No.桂科自 98110 0 7)
关键词
胃溃疡
细胞凋亡
表皮生长因子受体
细胞外信号调节激酶
SMAD3
免疫组织化学
幽门螺杆菌
gastric ulcer
apoptosis
epidermal growth factor receptor
SMAD3
extracellular signal-regulated kinase
immunohistochemical staining
helicobacter pylori
