论文部分内容阅读
目的研究亚硒酸钠对甲基硝基亚硝基胍（ＭＮＮＧ）所致胃粘膜细胞损伤的防护作用．方法观察了亚硒酸钠对ＭＮＮＧ所致胃粘膜细胞非程序ＤＮＡ合成（ＵＤＳ）、脂质过氧化物（ＬＰＯ）和ｒａｓＰ２１表达的影响．结果胃粘膜细胞先用１０μｍｏｌ／Ｌ或１μｍｏｌ／Ｌ亚硒酸钠预处理４ｈ，再给ＭＮＮＧ组细胞的非程序ＤＮＡ合成水平（ｃｐｍ／×１０－６ｍｉｎ－１，１１６６±１５６或１５６６±１８７ｖｓ１８３８±２０５，Ｐ＜００１～００５），脂质过氧化物（２０ｄ，μｍｏｌ／Ｌ，４５±０６或４７±０６ｖｓ７４±０７，Ｐ＜００１）和ｒａｓＰ２１蛋白含量（２０ｄ，Ａ，０６８±００８或０８６±００７ｖｓ１０８±０１１，Ｐ＜００１～００５）均显著低于ＭＮＮＧ组．结论一定剂量亚硒酸钠对ＭＮＮＧ诱导的胃粘膜细胞损伤有防护作用．
Objective To study the protective effect of sodium selenite on gastric mucosal cell injury induced by nitrobenzamide (MNNG). Methods The effects of sodium selenite on the expression of nonsynaptic DNA (UDS), lipid peroxides (LPO) and rasP21 in MNNG-induced gastric mucosal cells were observed. Results The gastric mucosal cells were pre-treated with 10μmol / L or 1μmol / L sodium selenite for 4h, then the non-procedural DNA synthesis (cpm / × 10-6min-1, 116.6 ± 15.6 or 1566 ± 187vs1838 ± 205, P <001 ~ 005), lipid peroxidation (20d, μmol / L, 45 ± 06 or 47 ± 0 6vs74 ± 07, P <001) and rasP21 protein content (20d, A, 068 ± 008 or 086 ± 007vs108 ± 011, P <0 01 ~ 005) were significantly lower than the MNNG group. Conclusion A certain dose of sodium selenite has a protective effect on MNNG-induced gastric mucosal cell injury.