氧化应激在间歇低氧诱导大鼠海马损伤中作用的研究

目的 探讨氧化应激在间歇低氧（IH）诱导大鼠海马损伤中的作用.方法 30只成年雄性Sprague-Dawley 大鼠随机分成对照组（CON组）、间歇低氧组（IH组）、Melatonin组（MEL组）,每组10只.采用化学比色法测定大鼠海马组织丙二醛（MDA）、超氧化物歧化酶（SOD）水平,并采取RT-PCR方法检测海马组织中Cu/Zn SOD、GPx、CAT的mRNA水平.结果 （1）在IH组中,MDA的水平为（1.68±0.23）μmol/g protein,均高于对照组和MEL组的（1.25±0.14）μmol/g protein和（1.35±0.18）μmol/g protein（P＜0.05或P＜0.01）;（2）在IH组中,SOD的活性、Cu/ZnSOD、GPx、CAT的mRNA表达水平分别为（43.01±4.96）103NU/g protein、0.25±0.02、0.34±0.09、0.38±0.03,均低于对照组和MEL组的（61.12±5.68）103NU/g protein和（55.98±4.65）103NU/g protein、0.48±0.06和0.43±0.08、0.55±0.07和0.54±0.05、0.57±0.04和0.53±0.07（P＜0.05,P＜0.01）.结论 间歇低氧可通过氧化应激导致大鼠海马损伤,MEL能抑制间歇缺氧导致的氧化应激,从而对间歇低氧大鼠海马损伤具有保护作用.

Study on the effect of oxidative stress on intermittent hypoxia induced-hippocampal injury in rats

Objective To explore the effect of oxidative stress on intermittent hypoxia induced-hip-pocampal injury in rats. Methods 30 adult male Sprague-Dawley rats were random divided into three groups ( 10 rats in each group), control group( CON group), intermittent group( IH group), and melatonin group( MEL group). The levels of MDA and SOD were detected by colorimetric method, and RT-PCR was used to examine the mRNA levels of the Cu/ZnSOD, GPx, CAT in hippocampal tissues. Results The level of MDA in IH group was ( 1. 68 ±0. 23) μmol/g, and it was obviously higher than that in control group (1.25±0.14)μmol/g and MEL group(1.35 ±0.18) μmoL/g ( P ＜0.05, P ＜0.01). In IH group, the activity of SOD and the mRNA levels of the Cu/ZnSOD,GPx and CAT were 43.01 ±4. 96 103NU/g, 0.25±0. 02,0. 34 ±0. 09,0. 38 ±0. 03 respectively, which were significantly lower than those in control group(61.12 ±5.68 103NU/g protein,0. 48 ±0.06,0. 55±0.07,0.57 ±0.04) and MEL group (55.98 ±4.65 103 NU/g,0.43 ± 0.08,0.54 ± 0.05,0.53 ± 0.07 ) ( P ＜ 0.05, P ＜ 0. 01 ). Conclusion Intermittent hypoxia can induce hippocampal injury in rats by oxidative stress, and melatonin can inhibit intermittent hypoxia induced-oxidant stress, so it can protect intermittent hypoxia induced-hippocampal injury in rats.