国际儿科学杂志
國際兒科學雜誌
국제인과학잡지
INTERNATIONAL JOURNAL OF PEDIATRICS
2008年
3期
199-201,封3
,共4页
马海燕%李向红%李红%张采欣%徐风森
馬海燕%李嚮紅%李紅%張採訢%徐風森
마해연%리향홍%리홍%장채흔%서풍삼
铅%模型,动物%胎盘%基质金属蛋白酶9%金属蛋白酶类组织抑制剂
鉛%模型,動物%胎盤%基質金屬蛋白酶9%金屬蛋白酶類組織抑製劑
연%모형,동물%태반%기질금속단백매9%금속단백매류조직억제제
Iead%Models Animal%Piaeenta%Matrix Metalloproteinase-9%Tissue Inhibitor of Melalloproteinases
目的 观察不同阶段铅暴露对孕鼠胎盘基质金属蛋白酶.9(MMP-9)及其组织抑制剂-1(TIMP-1)表达的影响,探讨铅的胎盘毒性机制.方法 108只大鼠随机分为4组,每组27只(雌雄比为2:1)合笼饲养,于孕期不同阶段饮服0.025%醋酸铅.对照组孕期全程(1~20d)饮服蒸馏水;实验A组孕早期(1~10d)饮服醋酸铅,孕后期(11~20d)饮服蒸馏水;实验B组孕早期(1~10d)饮服蒸馏水,孕后期(11~20d)饮服醋酸铅;实验C组孕期全程(1~20d)饮服醋酸铅.孕末期腹腔静脉取血,原子吸收光谱法测定血铅,免疫组化法测定胎盘滋养层细胞MMP-9和TIMP-1的表达.,结果 (1)对照组孕鼠孕末期平均血铅水平为(0.04±0.01)μmol/L,实验组孕鼠孕末期平均血铅水平均高于0.483μmol/L,实验C组血铅水平最高;(2)MMP-9和TIMP-1在胎盘组织中的表达部位主要位于滋养层细胞胞质;(3)胎盘滋养层细胞MMP-9表达4组问总体比较差异有统计学意义(x2=28.381,P<0.01),血铅水平最高的实验C组阳性表达率最低,与对照组比较差异有统计学意义(P<0.05);(4)胎盘滋养层细胞TIMP-1表达4组间总体比较差异有统计学意义(x2=18.177,P<0.05),表达强度以实验C组最高,实验A组次之,与对照组比较差异有统计学意义(P<0.05).结论 孕期MMP-9和TIMP-1的表达部位主要位于胎盘滋养层细胞.铅中毒程度越重,MMP-9和TIMP-1的表达强度改变越明显.MMP-9和TIMP-I的表达失衡可能是铅致胎盘损伤的病理机制之一.
目的 觀察不同階段鉛暴露對孕鼠胎盤基質金屬蛋白酶.9(MMP-9)及其組織抑製劑-1(TIMP-1)錶達的影響,探討鉛的胎盤毒性機製.方法 108隻大鼠隨機分為4組,每組27隻(雌雄比為2:1)閤籠飼養,于孕期不同階段飲服0.025%醋痠鉛.對照組孕期全程(1~20d)飲服蒸餾水;實驗A組孕早期(1~10d)飲服醋痠鉛,孕後期(11~20d)飲服蒸餾水;實驗B組孕早期(1~10d)飲服蒸餾水,孕後期(11~20d)飲服醋痠鉛;實驗C組孕期全程(1~20d)飲服醋痠鉛.孕末期腹腔靜脈取血,原子吸收光譜法測定血鉛,免疫組化法測定胎盤滋養層細胞MMP-9和TIMP-1的錶達.,結果 (1)對照組孕鼠孕末期平均血鉛水平為(0.04±0.01)μmol/L,實驗組孕鼠孕末期平均血鉛水平均高于0.483μmol/L,實驗C組血鉛水平最高;(2)MMP-9和TIMP-1在胎盤組織中的錶達部位主要位于滋養層細胞胞質;(3)胎盤滋養層細胞MMP-9錶達4組問總體比較差異有統計學意義(x2=28.381,P<0.01),血鉛水平最高的實驗C組暘性錶達率最低,與對照組比較差異有統計學意義(P<0.05);(4)胎盤滋養層細胞TIMP-1錶達4組間總體比較差異有統計學意義(x2=18.177,P<0.05),錶達彊度以實驗C組最高,實驗A組次之,與對照組比較差異有統計學意義(P<0.05).結論 孕期MMP-9和TIMP-1的錶達部位主要位于胎盤滋養層細胞.鉛中毒程度越重,MMP-9和TIMP-1的錶達彊度改變越明顯.MMP-9和TIMP-I的錶達失衡可能是鉛緻胎盤損傷的病理機製之一.
목적 관찰불동계단연폭로대잉서태반기질금속단백매.9(MMP-9)급기조직억제제-1(TIMP-1)표체적영향,탐토연적태반독성궤제.방법 108지대서수궤분위4조,매조27지(자웅비위2:1)합롱사양,우잉기불동계단음복0.025%작산연.대조조잉기전정(1~20d)음복증류수;실험A조잉조기(1~10d)음복작산연,잉후기(11~20d)음복증류수;실험B조잉조기(1~10d)음복증류수,잉후기(11~20d)음복작산연;실험C조잉기전정(1~20d)음복작산연.잉말기복강정맥취혈,원자흡수광보법측정혈연,면역조화법측정태반자양층세포MMP-9화TIMP-1적표체.,결과 (1)대조조잉서잉말기평균혈연수평위(0.04±0.01)μmol/L,실험조잉서잉말기평균혈연수평균고우0.483μmol/L,실험C조혈연수평최고;(2)MMP-9화TIMP-1재태반조직중적표체부위주요위우자양층세포포질;(3)태반자양층세포MMP-9표체4조문총체비교차이유통계학의의(x2=28.381,P<0.01),혈연수평최고적실험C조양성표체솔최저,여대조조비교차이유통계학의의(P<0.05);(4)태반자양층세포TIMP-1표체4조간총체비교차이유통계학의의(x2=18.177,P<0.05),표체강도이실험C조최고,실험A조차지,여대조조비교차이유통계학의의(P<0.05).결론 잉기MMP-9화TIMP-1적표체부위주요위우태반자양층세포.연중독정도월중,MMP-9화TIMP-1적표체강도개변월명현.MMP-9화TIMP-I적표체실형가능시연치태반손상적병리궤제지일.
Objective To explore the pathogenesis of placenta toxicity of lead exposure during different gestation periods by testing the blood lead level and the expression of mairix metalloproteimrse-9(MMP-9)and tissue inhibitor of metalloproteinase-1(11MP-1)in rat placenta.Methods108 Wistar rats(72 female,36 male)were randomly divi(1ed into four groups.All rats were orally fed with 0.025%lead acetate during different gestation periods.Blood was obtained from the abdominal vena cava and the lead level in matemal blood was measured by means of atomic absorption speclremetrv at the end of the pregnancy.The expression of MMP-9 and TIMP-1 in rat placenta was tested by means of immunohistochemistry.Results(1)The blood lead level in the end of pregnancy was 0.04μmol/L ±0.01 in control group.while jn experimental groups the blood lead levels were all higher than 0.483μmol/L,among them the highest blood lead level was in experimental group C.(2)The expression of MMP-9 and TIMP-1 mostly distilhated in trophoblastic cells.(3)The expression of MMP-9 had significant difference in four groups(x2=28.381,P<0.01).The expression of MMP-9 was significantly reduced in experimental group C(the highest blood lead level)compared with control group.(4)The expression of,TIMP-1 had significant difference in four groups(x2=18.177,P<0.05).The expresion of TIMP-1 was signifieantly increased in experimental group A、C compared with control group.Conclusions The expression of MMP-9 and TIMp-1 in rat placenta mosfly distributed in trophoblastic cells.They would change when the deglee of lead poisoning was more serious.The inbalance of expression of MMp-9/TIMP1 may play an important role in pathogenesis of placenta toxicity of lead exposure.