CAJ | 학술논문

目的观察小鼠海马不饱和脂肪酸含量变化,分析其在铅致小鼠学习记忆能力受损可能机制中的作用.方法 48只ICR小鼠分为4组,分别饮用0.625、1.250、2.500 g/L醋酸铅溶液50 d,同时设立对照组(饮用去离子水),水迷宫法测定小鼠学习记忆能力后,颈椎脱臼处死,取海马,高效液相色谱法测定小鼠海马中油酸(C18:1)、亚油酸(C18:2)、亚麻酸(C18:3)、花生四烯酸(C20:4,AA)、二十碳五烯酸(C20:5,EPA)和二十二碳六烯酸(C22:6,DHA)等6种不饱和脂肪酸的含量.结果 (1)在训练的第1～4天,中、高染铅组小鼠逃避潜伏期均明显长于对照组,在训练的第4天,低染铅组小鼠逃避潜伏期亦明显延长,差异有统计学意义(P＜0.05);第1～4天的逃避潜伏期均与染铅剂量呈明显的正相关,r值分别为0.973,0.985,0.929,0.936.(2)中、高剂量组小鼠海马C18:2和从较对照组明显上升;而C18:3、EPA、DHA较对照组明显下降,差异均有统计学意义(P＜0.05);高剂量组小鼠海马C18:1含量减少,差异有统计学意义(P＜0.01).逃避潜伏期与C18:1、C18:3、EPA、DHA呈负相关,与C18:2、AA呈正相关,r值分别为-0.901,-0.914,-0.893,-0.855,0.936,0.727.结论铅导致海马细胞脂肪酸代谢紊乱,使膜功能正常行使受阻,从而影响递质的合成、代谢和释放,导致学习记忆力的下降,推测这可能是铅干扰学习记忆能力的机制之一.
목적 관찰소서해마불포화지방산함량변화,분석기재연치소서학습기억능력수손가능궤제중적작용.방법 48지ICR소서분위4조,분별음용0.625、1.250、2.500 g/L작산연용액50 d,동시설립대조조(음용거리자수),수미궁법측정소서학습기억능력후,경추탈구처사,취해마,고효액상색보법측정소서해마중유산(C18:1)、아유산(C18:2)、아마산(C18:3)、화생사희산(C20:4,AA)、이십탄오희산(C20:5,EPA)화이십이탄륙희산(C22:6,DHA)등6충불포화지방산적함량.결과 (1)재훈련적제1～4천,중、고염연조소서도피잠복기균명현장우대조조,재훈련적제4천,저염연조소서도피잠복기역명현연장,차이유통계학의의(P＜0.05);제1～4천적도피잠복기균여염연제량정명현적정상관,r치분별위0.973,0.985,0.929,0.936.(2)중、고제량조소서해마C18:2화종교대조조명현상승;이C18:3、EPA、DHA교대조조명현하강,차이균유통계학의의(P＜0.05);고제량조소서해마C18:1함량감소,차이유통계학의의(P＜0.01).도피잠복기여C18:1、C18:3、EPA、DHA정부상관,여C18:2、AA정정상관,r치분별위-0.901,-0.914,-0.893,-0.855,0.936,0.727.결론 연도치해마세포지방산대사문란,사막공능정상행사수조,종이영향체질적합성、대사화석방,도치학습기억력적하강,추측저가능시연간우학습기억능력적궤제지일.
Objective To study possible impairment mechanisms of learning and memory abilities from unsaturated fatty acids in hippocampus of mice exposed to lead.Methods Forty-eight healthy mice were divided into 4 groups:low dose(0.625 g/L),middle dose(1.250 g/L) and high dose(2.500 g/L) of lead solution in diet and control group (distilled water).The mice in treatment groups were fed with lead solution every day while the mice in control group were fed with distilled water for 50 days.After learning and memory abilities were measured,the mice were killed and contents of oleic acid (C 18:1),linoleic acid (C 18:2),linolenic acid (C18:3),arachidonic acid (AA,C20:4),eicosapentaenoic acid (EPA,C20:5) and docosabexaenoie acid (DHA,C22:6) in hippocampus of mice were determined by high performance liquid chromatography (HPLC).Results (1) In the four training days,the mice treated with lead in the middle dose group and high dose group significantly increased the escape latencies compared with the mice treated with distilled water (P＜0.05) ,and on the 4th day,the low dosage mice' s escape latencies were delayed (P＜O.05).The escape latencies of the I st,2nd,3rd and 4th day had significantly positive linear relation with lead dose.Their relative coefficient in turn is r=0.973,0.985,0.929 and 0.936,indicating that lead harmed spatial memory of mice in Morris water maze (MWM).(2)The contents of C18:2 and AA were obviously enhanced in hippocampus of middle and high dosage (P＜0.05);while there was evident decrease in the contents of C 18:3,EPA and DHA (P＜0.05);the content of C 18:1 was decreased significantly in high dosage group (P＜0.01).The mice's escape latencies had significantly negative linear relation with contents of C 18:1,C 18:3,EPA and DHA,while there was positive linear relation significantly with contents of C18:2 and AA.Their relative coefficient in turn was r=-0.901,-0.914,-0.893,-0.855,0.936,0.727.Conclusion Lead interferes with the metabolism of hippocampus fatty acids and affects membrane function in hippocampus of mice,which might contribute to change of the synthesis,metabolism and release of central neurotransmitter and decrease of the learning and memory abilities.