中华临床营养杂志
中華臨床營養雜誌
중화림상영양잡지
CHINESE JOURNAL OF CLINICAL NUTRITION
2014年
5期
297-301
,共5页
谢慧%张京臣%陈莹%周飞%翁杰%章兵%吕东芝%龚裕强
謝慧%張京臣%陳瑩%週飛%翁傑%章兵%呂東芝%龔裕彊
사혜%장경신%진형%주비%옹걸%장병%려동지%공유강
ω-3多不饱和脂肪酸%急性肺损伤%肺湿干重比值%肺毛细血管通透指数%肺泡病理评分%核转录因子-κB%肿瘤坏死因子-α%白介素-1β
ω-3多不飽和脂肪痠%急性肺損傷%肺濕榦重比值%肺毛細血管通透指數%肺泡病理評分%覈轉錄因子-κB%腫瘤壞死因子-α%白介素-1β
ω-3다불포화지방산%급성폐손상%폐습간중비치%폐모세혈관통투지수%폐포병리평분%핵전록인자-κB%종류배사인자-α%백개소-1β
Omega-3 polyunsaturated fatty acids%Acute lung injury%Wet-to-dry ratio%Pulmonary vascular permeability index%Alveolar pathological score%Nuclear factor-κB%Tumor necrosis factor-α%Interleukin-1β
目的 评价ω-3多不饱和脂肪酸(3-PUFAs)对兔急性肺损伤(ALI)的保护作用.方法 60只雄性新西兰兔采用随机数字法分为3组,空白对照组(n=20)、3-PUFAs组(n=20)、ALI组(n=20).ALI组及3-PUFAs组兔注射乳化油酸建立ALI模型,空白对照组注射生理盐水乳化液.3-PUFAs组造模成功后连续静脉注射3-PUFAs,空白对照组和ALI组注射等量生理盐水.3组兔分别在造模成功后6、12、24、48 h各处死5只兔,观察和检测各组兔的肺湿干重比值、肺毛细血管通透指数、肺泡病理评分,取肺组织后采用逆转录多聚酶链反应法检测核转录因子-κB表达,蛋白质印迹法测定肿瘤坏死因子-α、白介素-1β蛋白表达情况.结果 在6、12、24、48 h,ALI组和空白对照组肺湿干重比(5.90±0.28比4.36±0.13;6.22 ±0.33比4.21±0.20;6.64 ±0.28比4.26±0.15;6.38±0.21比4.01±0.10;P均=0.000)、肺毛细血管通透性指数(22.11±1.52比8.21±1.12;26.57±1.53比8.10±0.86;24.32±1.29比7.95±1.52;23.64±0.82比7.87±0.81;P均=0.000)、弥漫性肺泡损伤系统评分(9.40±1.14比1.00±0.71;10.80±1.10比1.00±0.00; 12.00±0.71比1.00±1.00;12.40±0.55比0.80±0.45;P均=0.000)、核转录因子-κB(0.36±0.02比0.17 ±0.02; 0.30 ±0.02比0.18±0.02; 0.26±0.02比0.19±0.03; 0.26±0.02比0.17±0.02;P均=0.000)、肿瘤坏死因子-α(0.44±0.02比0.22±0.02;0.42±0.02比0.22±0.02;0.36±0.03比0.24±0.02;0.34±0.02比0.23±0.02;P均=0.000)、白介素-1β(0.35±0.02比0.19 ±0.03;0.34±0.03比0.17±0.05;0.29±0.03比0.19±0.03;0.26±0.02比0.19±0.04;P均=0.000)差异有统计学意义,病理损伤程度明显重于空白对照组;24、48 h时,3-PUFAs组与ALI组肺湿干重比(6.36±0.24比6.64±0.28;5.96±0.17比6.38±0.21;P=0.041,P=0.026)、肺毛细血管通透性指数(21.51±0.71比24.32±1.29; 19.92±1.19比23.64±0.82;P=0.003,P=0.001)、弥漫性肺泡损伤系统评分(10.40±0.89比12.00±0.71;10.60±1.14比12.40±0.55;P=0.009,P=0.024)、核转录因子-κB(0.23±0.01比0.26±0.02;0.23±0.01比0.26±0.02;P=0.001,P=0.001)、肿瘤坏死因子-d(0.34±0.02比0.36±0.03;0.32±0.02比0.34±0.02;P=0.006,P=0.001)、白介素-1β(0.25±0.02比0.29±0.03; 0.25±0.01比0.26±0.02; P=0.001,P=0.007)差异有统计学意义,病理损伤程度减轻.结论 ω-3多不饱和脂肪酸可改善急性肺损伤兔肺组织血管通透性并降低炎症因子水平,减轻ALI肺损伤程度.
目的 評價ω-3多不飽和脂肪痠(3-PUFAs)對兔急性肺損傷(ALI)的保護作用.方法 60隻雄性新西蘭兔採用隨機數字法分為3組,空白對照組(n=20)、3-PUFAs組(n=20)、ALI組(n=20).ALI組及3-PUFAs組兔註射乳化油痠建立ALI模型,空白對照組註射生理鹽水乳化液.3-PUFAs組造模成功後連續靜脈註射3-PUFAs,空白對照組和ALI組註射等量生理鹽水.3組兔分彆在造模成功後6、12、24、48 h各處死5隻兔,觀察和檢測各組兔的肺濕榦重比值、肺毛細血管通透指數、肺泡病理評分,取肺組織後採用逆轉錄多聚酶鏈反應法檢測覈轉錄因子-κB錶達,蛋白質印跡法測定腫瘤壞死因子-α、白介素-1β蛋白錶達情況.結果 在6、12、24、48 h,ALI組和空白對照組肺濕榦重比(5.90±0.28比4.36±0.13;6.22 ±0.33比4.21±0.20;6.64 ±0.28比4.26±0.15;6.38±0.21比4.01±0.10;P均=0.000)、肺毛細血管通透性指數(22.11±1.52比8.21±1.12;26.57±1.53比8.10±0.86;24.32±1.29比7.95±1.52;23.64±0.82比7.87±0.81;P均=0.000)、瀰漫性肺泡損傷繫統評分(9.40±1.14比1.00±0.71;10.80±1.10比1.00±0.00; 12.00±0.71比1.00±1.00;12.40±0.55比0.80±0.45;P均=0.000)、覈轉錄因子-κB(0.36±0.02比0.17 ±0.02; 0.30 ±0.02比0.18±0.02; 0.26±0.02比0.19±0.03; 0.26±0.02比0.17±0.02;P均=0.000)、腫瘤壞死因子-α(0.44±0.02比0.22±0.02;0.42±0.02比0.22±0.02;0.36±0.03比0.24±0.02;0.34±0.02比0.23±0.02;P均=0.000)、白介素-1β(0.35±0.02比0.19 ±0.03;0.34±0.03比0.17±0.05;0.29±0.03比0.19±0.03;0.26±0.02比0.19±0.04;P均=0.000)差異有統計學意義,病理損傷程度明顯重于空白對照組;24、48 h時,3-PUFAs組與ALI組肺濕榦重比(6.36±0.24比6.64±0.28;5.96±0.17比6.38±0.21;P=0.041,P=0.026)、肺毛細血管通透性指數(21.51±0.71比24.32±1.29; 19.92±1.19比23.64±0.82;P=0.003,P=0.001)、瀰漫性肺泡損傷繫統評分(10.40±0.89比12.00±0.71;10.60±1.14比12.40±0.55;P=0.009,P=0.024)、覈轉錄因子-κB(0.23±0.01比0.26±0.02;0.23±0.01比0.26±0.02;P=0.001,P=0.001)、腫瘤壞死因子-d(0.34±0.02比0.36±0.03;0.32±0.02比0.34±0.02;P=0.006,P=0.001)、白介素-1β(0.25±0.02比0.29±0.03; 0.25±0.01比0.26±0.02; P=0.001,P=0.007)差異有統計學意義,病理損傷程度減輕.結論 ω-3多不飽和脂肪痠可改善急性肺損傷兔肺組織血管通透性併降低炎癥因子水平,減輕ALI肺損傷程度.
목적 평개ω-3다불포화지방산(3-PUFAs)대토급성폐손상(ALI)적보호작용.방법 60지웅성신서란토채용수궤수자법분위3조,공백대조조(n=20)、3-PUFAs조(n=20)、ALI조(n=20).ALI조급3-PUFAs조토주사유화유산건립ALI모형,공백대조조주사생리염수유화액.3-PUFAs조조모성공후련속정맥주사3-PUFAs,공백대조조화ALI조주사등량생리염수.3조토분별재조모성공후6、12、24、48 h각처사5지토,관찰화검측각조토적폐습간중비치、폐모세혈관통투지수、폐포병리평분,취폐조직후채용역전록다취매련반응법검측핵전록인자-κB표체,단백질인적법측정종류배사인자-α、백개소-1β단백표체정황.결과 재6、12、24、48 h,ALI조화공백대조조폐습간중비(5.90±0.28비4.36±0.13;6.22 ±0.33비4.21±0.20;6.64 ±0.28비4.26±0.15;6.38±0.21비4.01±0.10;P균=0.000)、폐모세혈관통투성지수(22.11±1.52비8.21±1.12;26.57±1.53비8.10±0.86;24.32±1.29비7.95±1.52;23.64±0.82비7.87±0.81;P균=0.000)、미만성폐포손상계통평분(9.40±1.14비1.00±0.71;10.80±1.10비1.00±0.00; 12.00±0.71비1.00±1.00;12.40±0.55비0.80±0.45;P균=0.000)、핵전록인자-κB(0.36±0.02비0.17 ±0.02; 0.30 ±0.02비0.18±0.02; 0.26±0.02비0.19±0.03; 0.26±0.02비0.17±0.02;P균=0.000)、종류배사인자-α(0.44±0.02비0.22±0.02;0.42±0.02비0.22±0.02;0.36±0.03비0.24±0.02;0.34±0.02비0.23±0.02;P균=0.000)、백개소-1β(0.35±0.02비0.19 ±0.03;0.34±0.03비0.17±0.05;0.29±0.03비0.19±0.03;0.26±0.02비0.19±0.04;P균=0.000)차이유통계학의의,병리손상정도명현중우공백대조조;24、48 h시,3-PUFAs조여ALI조폐습간중비(6.36±0.24비6.64±0.28;5.96±0.17비6.38±0.21;P=0.041,P=0.026)、폐모세혈관통투성지수(21.51±0.71비24.32±1.29; 19.92±1.19비23.64±0.82;P=0.003,P=0.001)、미만성폐포손상계통평분(10.40±0.89비12.00±0.71;10.60±1.14비12.40±0.55;P=0.009,P=0.024)、핵전록인자-κB(0.23±0.01비0.26±0.02;0.23±0.01비0.26±0.02;P=0.001,P=0.001)、종류배사인자-d(0.34±0.02비0.36±0.03;0.32±0.02비0.34±0.02;P=0.006,P=0.001)、백개소-1β(0.25±0.02비0.29±0.03; 0.25±0.01비0.26±0.02; P=0.001,P=0.007)차이유통계학의의,병리손상정도감경.결론 ω-3다불포화지방산가개선급성폐손상토폐조직혈관통투성병강저염증인자수평,감경ALI폐손상정도.
Objective To evaluate the protective effect of ω-3 polyunsaturated fatty acids (3-PUFAs)on acute lung injury (ALI) in rabbits.Methods Sixty male New Zcaland rabbits were divided into 3 groups with random number table,i.e.blank control group (n =20),3-PUFAs group (n =20),and ALI group (n =20).The rabbits in the ALI group and the 3-PUFAs group were injected with emulsified oleic acid to build an ALI model,while the rabbits in the blank control group were injected with saline emulsion.After building ALI model,the rabbits in the 3-PUFAs group were intravenously injected with 3-PUFAs solution,and the rabbits in the blank control group and the ALI group were injected with normal saline solution of the same volume.5 rabbits were killed in each group at each of 4 time points after building ALI model (6 hours,12 hours,24 hours,and 48 hours).We observed the changes in lung wet-to-dry weight ratio,pulmonary vascular permeability index,alveolar pathology score.The expression of nuclear factor-κB in lung tissue of the rabbits was detected by reverse transcription polymerase chain reaction,expressions of tumor necrosis factor-α and interleukin-1 β protein by Western blot.Results At 6,12,24,and 48 hours after modeling,compared with the blank control group,the ALI group exhibited significantly higher wet-to-dry ratio (5.90 ± 0.28 vs.4.36 ± 0.13,6.22 ±0.33 vs.4.21 ±0.20,6.64±0.28 vs.4.26±0.15,6.38±0.21 vs.4.01±0.10,allP=0.000),pulmonary vascular permeability index (22.11 ± 1.52 vs.8.21 ± 1.12,26.57 ± 1.53 vs.8.10 ± 0.86,24.32 ±1.29 vs.7.95 ± 1.52,23.64 ±0.82 vs.7.87 ±0.81,all P =0.000),diffuse alveolar damage score (9.40 ±1.14 vs.1.00±0.71,10.80±1.10vs.1.00±0.00,12.00±0.71 vs.1.00±1.00,12.40±0.55vs.0.80±0.45,all P =0.000),nuclear factor-κB mRNA expression (0.36 ± 0.02 vs.0.17 ± 0.02,0.30 ± 0.02 vs.0.18 ±0.02,0.26 ±0.02 vs.0.19 ±0.03,0.26 ±0.02 vs.0.17 ±0.02,all P =0.000),tumor necrosis factor-α expression (0.44 ± 0.02 vs.0.22 ± 0.02,0.42 ± 0.02 vs.0.22 ± 0.02,0.36 ± 0.03 vs.0.24 ±0.02,0.34 ±0.02 vs.0.23 ±0.02,all P =0.000),and interleukin-1β expression (0.35 ±0.02 vs.0.19 ±0.03,0.34±0.03 vs.0.17±0.05,0.29±0.03 vs.0.19±0.03,0.26 ±0.02 vs.0.19±0.04,allP=0.000),showing an obviously more severe pathological injury.At 24 and 48 hours after modeling,compared with the ALI group,the 3-PUFAs group had lower wet-to-dry ratio (6.36 ±0.24 vs.6.64 ±0.28,P =0.041 ;5.96 ±0.17 vs.6.38 ±0.21,P =0.026),pulmonary vascular permeability index (21.51 ±0.71 vs.24.32 ±1.29,P =0.003 ; 19.92 ± 1.19 vs.23.64 ±0.82,P =0.001),diffuse alveolar damage score (10.40 ±0.89vs.12.00 ± 0.71,P =0.009 ; 10.60 ± 1.14 vs.12.40 ± 0.55,P =0.024),nuclear factor-κB mRNA expression (0.23 ± 0.01 vs.0.26 ± 0.02,P =0.001 ; 0.23 ± 0.01 vs.0.26 ± 0.02,P =0.001),tumor necrosis factor-α expression (0.34 ±0.02 vs.0.36 ± 0.03,P =0.006; 0.32 ± 0.02 vs.0.34 ± 0.02,P =0.001),and interleukin-1 β expression (0.25 ±0.02 vs.0.29 ±0.03,P =0.001 ; 0.25 ±0.01 vs.0.26 ±0.02,P=0.007),showing a lighter pathological injury.Conclusion 3-PUFAs may relieve ALI in rabbits through reducing pulmonary vascular permeability and levels of inflammatory factors.
