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目的和方法：采用人胃粘膜上皮细胞系ＧＥＳ１细胞传代培养技术，利用Ｆｅ２＋与Ｈ２Ｏ２反应生成的羟自由基（ｈｙｄｒｏｘｙｌｒａｄｉｃａｌ，ＯＨ·）建立细胞损伤模型，探讨ＯＨ·损伤人胃粘膜细胞的机制，观察生长抑素（ｓｏｍａｔｏｓｔａｔｉｎ，ＳＳ）对ＧＥＳ１细胞抗ＯＨ·损伤的影响。结果：（１）ＯＨ·可直接损伤ＧＥＳ１细胞，表现为细胞存活率下降而细胞乳酸脱氢酶（ｌａｃｔａｔｅｄｅｈｙｄｒｏｇｅｎａｓｅ，ＬＤＨ）漏出量增多；预先在细胞培养液中加入ＯＨ·特异性清除剂二甲基亚砜（５ｍｍｏｌ／Ｌ），可预防该损伤。预先加入ＳＳ（０．０１ｍｇ／Ｌ，０．１ｍｇ／Ｌ，１．０ｍｇ／Ｌ，１０ｍｇ／Ｌ）对细胞存活率和细胞ＬＤＨ漏出量无影响；（２）加入ＯＨ·后，细胞丙二醛（ＭＤＡ）、氧化型谷胱甘肽（ＧＳＳＧ）含量上升而还原型谷胱甘肽（ＧＳＨ）含量下降。以ＳＳ０．１ｍｇ／Ｌ，１．０ｍｇ／Ｌ，１０ｍｇ／Ｌ预处理，可部分减轻上述改变。结论：ＯＨ·可直接损伤ＧＥＳ１细胞，其机制与破坏细胞的巯基稳态及加重细胞的脂质过氧化程度有关；ＳＳ可通过维持细胞的巯基稳态，部分减轻ＯＨ·所致的ＧＥＳ１细胞脂质过氧化程度。
Objective and Methods: The human gastric epithelial cell line GES 1 cell subculturing technology, the use of Fe2 + and H2O2 reaction of hydroxyl radicals (hydroxylradical, OH ·) to establish a cell injury model to explore the OH · damage of human gastric mucosal cells , Observe the effect of somatostatin (SS) on the anti-OH · injury of GES1 cells. Results: (1) OH · could directly damage GES1 cells, showing the decrease of cell viability and the increase of cell lactate dehydrogenase (LDH) leakage; adding OH · specific scavenger II Methyl sulfoxide (5 mmol / L) prevented this injury. Pretreatment with SS (0.01 mg / L, 0.1 mg / L, 1.0 mg / L, 10 mg / L) had no effect on cell viability and LDH leakage; (2) MDA, GSSG and GSH decreased. With SS0.1mg / L, 1.0mg / L, 10mg / L pretreatment, can partially reduce the above changes. Conclusions: OH · can directly damage GES-1 cells, and its mechanism is related to the destruction of the cell’s sulfhydryl steady state and aggravating the cell’s lipid peroxidation. SS can partially reduce the OH · -dependent GES by maintaining the sulfhydryl steady state of cells 1 cell lipid peroxidation.