丁酸钠对甲基硝基亚硝基胍所致胃粘膜上皮细胞非程序DNA合成、脂质过氧化和rasp21表达的影响  

Preventive effects of sodium butyrate on gastric epithelial cells damaged by N-methyl-N’-nitro-N-nitrosoguanidine

作　　者：刘卫[1] 朱斌[1] 房殿春[2] 

机构地区：[1]解放军第105医院消化科,合肥230031 [2]第三军医大学西南医院全军消化内科中心,重庆400038

出　　处：《第三军医大学学报》2005年第20期2057-2059,共3页Journal of Third Military Medical University

摘　　要：目的观察丁酸钠(sodiumbutyrate,SB)对甲基硝基亚硝基胍(NmethylN′nitroNnitrocoguanidine,MNNG)所致胃粘膜上皮细胞非程序DNA合成、脂质过氧化和rasp21表达的影响。方法分4组:MNNG、10-5mol/LSB+MNNG、10-6mol/LSB+MNNG、10-7mol/LSB+MNNG,各组测定UDS、LPO和rasp21蛋白。结果胃粘膜细胞先用10-5mol/L、10-6mol/L丁酸钠预处理4h,再给MNNG,细胞非程序DNA合成水平、脂质过氧化和rasp21蛋白含量均显著低于MNNG组(P<0.05,P<0.01)。结论一定剂量丁酸钠对MNNG诱导的胃粘膜细胞损伤有保护作用。Objective To investigate the effects of sodium butyrate （SB） on fetal gastric epithelial cells （GECs） in vitro damaged by N-methyl-N＇ -nitro-N-nitrosoguanidine （MNNG）. Methods The fetal gastric epithelial cells were isolated, cultured and identified. Then the cells of the second generation were cocultured with 10^-5 mol/L, 10^-6 mol/L, 10^-7 mol/L SB for 4 h, then added with 10^-5 mol/L MNNG culturing for another 24 h. After the treated cells were finally cultured in normal culture medium for 40 d, the unscheduled DNA synthesis （UDS）, lipid peroxidation （LPO） and ras p21 were detected. The cells were only cultured with 10^-5 mol/L MNNG served as negative control and without MNNG or SB as normal control. Results The level of UDS, the contents of lipid peroxidation products and the concentrations of ras p21 in GECs treated with 10^-5 mol/L and 10^-6 mol/L SB decreased obviously, and had significant differences with that of GECs treated without SB. Conclusion SB can effectively prevent the damage of GECs induced from MNNG.

关 键 词：胃粘膜上皮细胞 甲基硝基亚硝基胍 丁酸钠 

分 类 号：R730.23[医药卫生—肿瘤] R735.2[医药卫生—临床医学]