南方医科大学学报

南方医科大学学报 ›› 2006, Vol. 26 ›› Issue (08): 1190-1193.

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酸对人正常食管粘膜上皮细胞增殖和ERK表达水平的影响

姜志茹； 龚均； 乔哲； 张珍妮；   

  1. 西安交通大学第二医院消化科； 西安交通大学第二医院胸外科； 西安交通大学第二医院麻醉科 陕西西安710004； 陕西西安710004；
  • 出版日期:2006-08-20 发布日期:2006-08-20

Temporary acid exposure promotes normal human esophageal epithelial cell proliferation and ERK expression in vitro

JIANG Zhi-ru1, GONG Jun1, QIAO Zhe2, ZHANG Zhen-ni3 Departments of Gastroenterology1, Thoracic Surgery2 and Anesthesiology3, Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, China   

  1. 西安交通大学第二医院消化科； 西安交通大学第二医院胸外科； 西安交通大学第二医院麻醉科 陕西西安710004； 陕西西安710004；
  • Online:2006-08-20 Published:2006-08-20

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摘要： 目的观察酸对人正常食管粘膜上皮细胞的增殖和细胞外信号调节蛋白激酶(ERK)表达水平的影响。方法体外培养人正常食管粘膜上皮细胞,分别在pH4.0￣6.5的条件下培养3￣60min并设对照(pH7.3)进行比较。采用MTT法和流式细胞技术测定细胞增殖状态。免疫印迹法测定磷酸化ERK1/2蛋白表达。结果酸的短时间(3min)作用使细胞增殖比大于1,S期细胞比率升高,磷酸化ERK1/2蛋白表达增加。当酸作用时间大于6min时,细胞增殖比小于1,S期细胞比率下降。ERK抑制剂U0126可阻断酸诱导的细胞增殖。结论酸的短时间刺激可促进人正常食管细胞的增殖,与ERK表达上调有关。 

Abstract: Objective To observe the effects of temporary acid exposure on cell proliferation and extracellular signal-regulated protein kinase (ERK) activity in normal human esophageal epithelial cells in vitro. Methods Normal human esophageal epithelial cells cultured in vitro were exposed to acidic media (pH 4.0-6.5) for 3 to 60 min, and the control cells were cultured at pH 7.3. MTT assay and flow cytometry were employed for cell proliferation assessment. The expression of phosphorylated ERK1/2 protein was determined by immunoblotting. Results Esophageal epithelial cells with acid exposure for 3 min exhibited a significant increase in cell proliferation, increased number of cells in S phase and enhanced expression of phosphorylated ERK1/2 protein. Acid exposure of the esophageal epithelial cells exceeding 6 min resulted in depressed proliferation and decreased S-phase cells, and cell proliferation induced by acid exposure was abolished by pretreatment with U0126. Conclusion Temporary acid stimulus increases cell proliferation of normal human esophageal epithelial cells in vitro by activating the ERK pathway.

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