中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2014年
2期
84-88
,共5页
谷振勇%陈良%李娅%薛莉%谢小萍%任杰%李金声%王文岚
穀振勇%陳良%李婭%薛莉%謝小萍%任傑%李金聲%王文嵐
곡진용%진량%리아%설리%사소평%임걸%리금성%왕문람
急性一氧化碳中毒%免疫炎症反应%巨噬细胞
急性一氧化碳中毒%免疫炎癥反應%巨噬細胞
급성일양화탄중독%면역염증반응%거서세포
Acute carbon monoxide poisoning%Immune inflammatory reaction%Macrophages
目的 探讨急性一氧化碳(CO)中毒大鼠脑组织损伤中巨噬细胞介导的非特异性免疫反应.方法 清洁级雄性SD大鼠24只,按数字表法随机分为正常对照组(对照组)、CO中毒3d组(中毒3d组)和CO中毒7d组(中毒7d组),每组8只.中毒3d组和中毒7d组建立急性CO中毒大鼠模型,中毒3d组于建模后3d、对照组和中毒7d组于建模后7d腹腔麻醉后灌注、取脑,应用电镜、免疫组织化学染色和免疫印记等方法观察各组脑组织超微结构的改变、巨噬细胞的浸润以及相关细胞因子的表达.结果 电镜下,急性CO中毒后的大鼠脑组织,神经元发生变性坏死、小胶质细胞聚集在损伤神经元周围;脑内有巨噬细胞浸润、巨噬细胞炎性蛋白-1α(MIP-1 α)和细胞间黏附分子-1(ICAM-1)的表达.对照组巨噬细胞特异性蛋白(ED-1)表达较少,5个高倍视野内阳性细胞数,皮层(2.83±1.72)个,海马(2.33±1.37)个;中毒7d组表达最显著,皮层(30.33 ±1.14)个,海马(16.00±1.41)个,与对照组比较差异均有统计学意义(P＜0.01).对照组MIP-1α表达较少,5个高倍视野内阳性细胞数,皮层(5.83±2.48)个,海马(6.67±2.94)个;中毒3d组表达最显著,皮层(238.33±11.94)个,海马(207.83±9.79)个,与对照组比较差异均有统计学意义(P＜0.01).ICAM-1表达趋势与MIP-1α一致,对照组表达较少,全脑5个高倍视野内积分光密度值(IOD)为10.56±16.11;中毒3d组表达最显著,IOD为845.77±80.70,与对照组比较差异有统计学意义(P＜0.01).结论 急性CO中毒大鼠脑损伤后,有巨噬细胞介导的非特异性免疫炎症反应参与,且这一反应可能与细胞因子的趋化作用有关.
目的 探討急性一氧化碳(CO)中毒大鼠腦組織損傷中巨噬細胞介導的非特異性免疫反應.方法 清潔級雄性SD大鼠24隻,按數字錶法隨機分為正常對照組(對照組)、CO中毒3d組(中毒3d組)和CO中毒7d組(中毒7d組),每組8隻.中毒3d組和中毒7d組建立急性CO中毒大鼠模型,中毒3d組于建模後3d、對照組和中毒7d組于建模後7d腹腔痳醉後灌註、取腦,應用電鏡、免疫組織化學染色和免疫印記等方法觀察各組腦組織超微結構的改變、巨噬細胞的浸潤以及相關細胞因子的錶達.結果 電鏡下,急性CO中毒後的大鼠腦組織,神經元髮生變性壞死、小膠質細胞聚集在損傷神經元週圍;腦內有巨噬細胞浸潤、巨噬細胞炎性蛋白-1α(MIP-1 α)和細胞間黏附分子-1(ICAM-1)的錶達.對照組巨噬細胞特異性蛋白(ED-1)錶達較少,5箇高倍視野內暘性細胞數,皮層(2.83±1.72)箇,海馬(2.33±1.37)箇;中毒7d組錶達最顯著,皮層(30.33 ±1.14)箇,海馬(16.00±1.41)箇,與對照組比較差異均有統計學意義(P＜0.01).對照組MIP-1α錶達較少,5箇高倍視野內暘性細胞數,皮層(5.83±2.48)箇,海馬(6.67±2.94)箇;中毒3d組錶達最顯著,皮層(238.33±11.94)箇,海馬(207.83±9.79)箇,與對照組比較差異均有統計學意義(P＜0.01).ICAM-1錶達趨勢與MIP-1α一緻,對照組錶達較少,全腦5箇高倍視野內積分光密度值(IOD)為10.56±16.11;中毒3d組錶達最顯著,IOD為845.77±80.70,與對照組比較差異有統計學意義(P＜0.01).結論 急性CO中毒大鼠腦損傷後,有巨噬細胞介導的非特異性免疫炎癥反應參與,且這一反應可能與細胞因子的趨化作用有關.
목적 탐토급성일양화탄(CO)중독대서뇌조직손상중거서세포개도적비특이성면역반응.방법 청길급웅성SD대서24지,안수자표법수궤분위정상대조조(대조조)、CO중독3d조(중독3d조)화CO중독7d조(중독7d조),매조8지.중독3d조화중독7d조건립급성CO중독대서모형,중독3d조우건모후3d、대조조화중독7d조우건모후7d복강마취후관주、취뇌,응용전경、면역조직화학염색화면역인기등방법관찰각조뇌조직초미결구적개변、거서세포적침윤이급상관세포인자적표체.결과 전경하,급성CO중독후적대서뇌조직,신경원발생변성배사、소효질세포취집재손상신경원주위;뇌내유거서세포침윤、거서세포염성단백-1α(MIP-1 α)화세포간점부분자-1(ICAM-1)적표체.대조조거서세포특이성단백(ED-1)표체교소,5개고배시야내양성세포수,피층(2.83±1.72)개,해마(2.33±1.37)개;중독7d조표체최현저,피층(30.33 ±1.14)개,해마(16.00±1.41)개,여대조조비교차이균유통계학의의(P＜0.01).대조조MIP-1α표체교소,5개고배시야내양성세포수,피층(5.83±2.48)개,해마(6.67±2.94)개;중독3d조표체최현저,피층(238.33±11.94)개,해마(207.83±9.79)개,여대조조비교차이균유통계학의의(P＜0.01).ICAM-1표체추세여MIP-1α일치,대조조표체교소,전뇌5개고배시야내적분광밀도치(IOD)위10.56±16.11;중독3d조표체최현저,IOD위845.77±80.70,여대조조비교차이유통계학의의(P＜0.01).결론 급성CO중독대서뇌손상후,유거서세포개도적비특이성면역염증반응삼여,차저일반응가능여세포인자적추화작용유관.
Objective To investigate the effect of nonspecific immune reaction mediated by macrophages on brain injury induced by acute carbon monoxide (CO) poisoning in rats.Methods Twenty-four male healthy rats were randomly divided into the 3 days after CO poisoning group (or group A),the 7 days after CO poisoning group (or group B) and the normal control group (or group C),each consisting of 8 animals.Models of acute CO poisoning were established by using the animals in group A and group B.Samples of the brain tissue were collected following abdominal anesthesia.Electron microscopy,immunohistochemistry and Western blot were used to observe changes in ultra-structure of the brain tissue,infiltration of macrophages and the expression of related cytokines.Results Following acute CO poisoning,neuronal degeneration,necrosis and microglia accumulation around the injured neurons could be observed under electron microscopy.Macrophage infiltration and expressions of macrophage inflammatory protein-1α (MIP-1 α) and intercellular adhesion molecule-1 (ICAM-1) were observed in the brain of rats,while for the animals in the control group,there was little expression of macrophage specific protein (ED-1).The No.of positive cells in the cortex was 2.83 ± 1.72,and the No.of positive cells in the hippocampus was 2.33 ± 1.37.The peak of macrophage infiltration was seen 7 days after CO poisoning,with the No.of positive cells in the cortex being 30.33 ± 1.14 and the No.of positive cells in the hippocampus being 16.00 ± 1.41.Statistical significance could be seen,as compared with those of the control group (P ＜ 0.05).However,there was little the expression of MIP-1 α in the control group.Under the electron microscope,the No.of positive cells in the cortex was 5.83 ± 2.48 and the No.of positive cells in the hippocampus was 6.67 ±2.94.The expression of MIP-1α for group A was most significant,with the No.of positive cells in the cortex being 238.33 ± 11.94 and the No.of positive cells in the hippocampus being 207.83 ± 9.79.Statistical significance could be noted,when comparisons were made with the control group(P ＜0.01).The trend in expression of ICAM-1 was identical to that of MIP-1α,but little expression of ICAM-1 could be seen in the control group,with IOD in total brain being 10.56 ± 16.11.The expression for group A was most significant,with IOD in total brain being 845.77 ± 80.70.And statistical significance could be noted,when comparisons were made with the control group(P ＜0.01).Conclusions Nonspecific immune reaction mediated by macrophages was involved in brain injury,following acute CO poisoning,and the reaction might be associated with the chemotactic effect of cytokines.
