中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2011年
8期
1247-1249
,共3页
祁海杰%夏军%王志维%戴飞锋%徐鹏%罗彬
祁海傑%夏軍%王誌維%戴飛鋒%徐鵬%囉彬
기해걸%하군%왕지유%대비봉%서붕%라빈
肺%缺血后处理%钾通道
肺%缺血後處理%鉀通道
폐%결혈후처리%갑통도
Lung%Ischemic postconditioning%Potassium channel
目的 探讨缺血后处理(IPO)对大鼠在体肺缺血-再灌注损伤(I/R)的保护作用及线粒体ATP敏感性钾通道(mitoKATP)在缺血后处理效应中的作用.方法 将Wistar大鼠35只随机分为5组:假手术组(Sham组)、缺血再灌注损伤组(I/R组)、缺血后处理组(IPO组)、缺血再灌注损伤+5-羟基葵酸盐组(I/R+5-HD组)、缺血后处理+5-羟基葵酸盐组(IPO+5-HD组).观察各组肺组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、湿/干比值(W/D)以及病理形态学改变.结果 I/R组与Sham组比较MDA含量增加[(5.07±1.60)nmol/mg prot比(1.43±0.41)nmol/mgprot,P＜0.01],SOD活性减低[(12.38±2.24)U/mg prot比(45.51±5.42)U/mg prot,P＜0.01],W/D比值增高(5.45±0.82比3.05±0.47,P＜0.01),肺组织形态及超微结构明显受损;IPO+5-HD组与IPO组比较MDA含量增加[(3.74±0.71)nmol/mg prot比(2.60±0.43)nmol/mg prot,P＜0.01],SOD活性减低[(22.91±2.71)U/mg prot比(28.74±2.03)U/mg prot,P＜0.01],W/D比值增高(4.64±0.79比3.89±0.60,P＜0.01),肺组织形态及超微结构明显受损;IPO组与I/R组比较,肺组织MDA含量减少[(2.60±0.43)nmol/mg prot比(5.07±1.60)nmol/mg prot,P＜0.01],SOD活性增高[(28.74±2.03)U/mg prot比(12.38±2.24)U/mg prot,P＜0.01],W/D比值减低(3.89±0.60比5.45±0.82,P＜0.01),肺组织病理形态学改变轻于I/R组;I/R+5-HD组与I/R组比较,肺组织MDA含量[(5.14±1.30)mol/mg prot比(5.07±1.60)mol/mg prot,P＞0.05)、SOD活性[(11.65±1.82)U/mg prot比(12.38±2.24)U/mg prot,P＞0.05]、W/D比变化(5.54±0.61比5.45±0.82),差异无统计学意义(P＞0.05),肺组织病理形态学改变无明显差异.IPO+5-HD组的各项指标介于IPO组和I/R组之间.结论 缺血后处理能减轻大鼠在体肺缺血再灌注损伤,mitoKATP参与了肺缺血后处理效应.
目的 探討缺血後處理(IPO)對大鼠在體肺缺血-再灌註損傷(I/R)的保護作用及線粒體ATP敏感性鉀通道(mitoKATP)在缺血後處理效應中的作用.方法 將Wistar大鼠35隻隨機分為5組:假手術組(Sham組)、缺血再灌註損傷組(I/R組)、缺血後處理組(IPO組)、缺血再灌註損傷+5-羥基葵痠鹽組(I/R+5-HD組)、缺血後處理+5-羥基葵痠鹽組(IPO+5-HD組).觀察各組肺組織中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、濕/榦比值(W/D)以及病理形態學改變.結果 I/R組與Sham組比較MDA含量增加[(5.07±1.60)nmol/mg prot比(1.43±0.41)nmol/mgprot,P＜0.01],SOD活性減低[(12.38±2.24)U/mg prot比(45.51±5.42)U/mg prot,P＜0.01],W/D比值增高(5.45±0.82比3.05±0.47,P＜0.01),肺組織形態及超微結構明顯受損;IPO+5-HD組與IPO組比較MDA含量增加[(3.74±0.71)nmol/mg prot比(2.60±0.43)nmol/mg prot,P＜0.01],SOD活性減低[(22.91±2.71)U/mg prot比(28.74±2.03)U/mg prot,P＜0.01],W/D比值增高(4.64±0.79比3.89±0.60,P＜0.01),肺組織形態及超微結構明顯受損;IPO組與I/R組比較,肺組織MDA含量減少[(2.60±0.43)nmol/mg prot比(5.07±1.60)nmol/mg prot,P＜0.01],SOD活性增高[(28.74±2.03)U/mg prot比(12.38±2.24)U/mg prot,P＜0.01],W/D比值減低(3.89±0.60比5.45±0.82,P＜0.01),肺組織病理形態學改變輕于I/R組;I/R+5-HD組與I/R組比較,肺組織MDA含量[(5.14±1.30)mol/mg prot比(5.07±1.60)mol/mg prot,P＞0.05)、SOD活性[(11.65±1.82)U/mg prot比(12.38±2.24)U/mg prot,P＞0.05]、W/D比變化(5.54±0.61比5.45±0.82),差異無統計學意義(P＞0.05),肺組織病理形態學改變無明顯差異.IPO+5-HD組的各項指標介于IPO組和I/R組之間.結論 缺血後處理能減輕大鼠在體肺缺血再灌註損傷,mitoKATP參與瞭肺缺血後處理效應.
목적 탐토결혈후처리(IPO)대대서재체폐결혈-재관주손상(I/R)적보호작용급선립체ATP민감성갑통도(mitoKATP)재결혈후처리효응중적작용.방법 장Wistar대서35지수궤분위5조:가수술조(Sham조)、결혈재관주손상조(I/R조)、결혈후처리조(IPO조)、결혈재관주손상+5-간기규산염조(I/R+5-HD조)、결혈후처리+5-간기규산염조(IPO+5-HD조).관찰각조폐조직중병이철(MDA)함량、초양화물기화매(SOD)활성、습/간비치(W/D)이급병리형태학개변.결과 I/R조여Sham조비교MDA함량증가[(5.07±1.60)nmol/mg prot비(1.43±0.41)nmol/mgprot,P＜0.01],SOD활성감저[(12.38±2.24)U/mg prot비(45.51±5.42)U/mg prot,P＜0.01],W/D비치증고(5.45±0.82비3.05±0.47,P＜0.01),폐조직형태급초미결구명현수손;IPO+5-HD조여IPO조비교MDA함량증가[(3.74±0.71)nmol/mg prot비(2.60±0.43)nmol/mg prot,P＜0.01],SOD활성감저[(22.91±2.71)U/mg prot비(28.74±2.03)U/mg prot,P＜0.01],W/D비치증고(4.64±0.79비3.89±0.60,P＜0.01),폐조직형태급초미결구명현수손;IPO조여I/R조비교,폐조직MDA함량감소[(2.60±0.43)nmol/mg prot비(5.07±1.60)nmol/mg prot,P＜0.01],SOD활성증고[(28.74±2.03)U/mg prot비(12.38±2.24)U/mg prot,P＜0.01],W/D비치감저(3.89±0.60비5.45±0.82,P＜0.01),폐조직병리형태학개변경우I/R조;I/R+5-HD조여I/R조비교,폐조직MDA함량[(5.14±1.30)mol/mg prot비(5.07±1.60)mol/mg prot,P＞0.05)、SOD활성[(11.65±1.82)U/mg prot비(12.38±2.24)U/mg prot,P＞0.05]、W/D비변화(5.54±0.61비5.45±0.82),차이무통계학의의(P＞0.05),폐조직병리형태학개변무명현차이.IPO+5-HD조적각항지표개우IPO조화I/R조지간.결론 결혈후처리능감경대서재체폐결혈재관주손상,mitoKATP삼여료폐결혈후처리효응.
Objective To investigate the protective effect of ischemic postconditioning (IPO) on lung ischemic reperfusion (L/R) in rats in vivo and the mechanism of mitochondrial ATP-sensitive potassium channel (mitoKATP) blocker in the ischemic postconditioning. Methods Thirty five Wistar rats were randomly divided into 5 groups: sham group, I/R group, ischemic postconditioning (IPO) group, I/R +5-hydroxydecanoate (I/R + 5-HD) group, IPO + 5-HD group. The concentration of malondialdehyde (MDA) and activity of superoide dismutase (SOD) were determined in the lung homogenate, wet to dry weight ratio (W/D) was measured and pathological changes were also observed. Results The levels of MDA[(5.07±1.60) vs (1.43 ±0.41) nmol/mg prot,P＜0. 01]and W/D (5.45 ±0.82 vs 3.05 ±0. 47,P ＜0. 01 ) were increased significantly in I/R group as compared with sham group, while the activity of SOD[( 12. 38 ±2. 24) vs (45.51 ±5.42) U/mg prot,P ＜0. 01]was decreased, and the injury of lung tissues was significantly aggravated in IPO + 5-HD group as compared with IPO group[MDA: (3.74 ±0. 71 ) nmol/mg prot vs (2. 60 ± 0. 43 ) nmol/mg prot , P ＜ 0. 01]; W/D: 4. 64 ± 0. 79 vs 3. 89 ± 0. 60,P＜0.01; SOD:[(22.91 ±2.71) U/mg prot vs (28.74±2.03) U/mg prot,P＜0. 01]. The levels of MDA[(2.60±0.43) vs (5.07 ±1.60) nmol/mg prot,P＜0. 01]and W/D (3.89 ±0.60 vs 5.45 ±0. 82,P ＜0. 01 ) were decreased significantly in IPO group as compared with I/R group, the activity of SOD[(28.74±2.03) vs (12.38 ±2.24) U/mg prot,P＜0. 01]increased and lung tissue histological damage attenuated. The difference in MDA[(5.14 ± 1.30) vs (5.07 ± 1.60) nmol/mg prot, P ＞ 0. 05],W/D (5.54±0.61 vs5.45 ±0.82,P＞0.05) and SOD[(11.65 ±1.82) vs (12.38 ±2.24) U/mgprot,P ＞ 0. 05]levels had no statistical significance between I/R + 5-HD group and I/R group, and the injury of lung tissues had no significant difference too. Each index in IPO + 5-HD group was between IPO and I/R groups. Conclusion Ischemic postconditioning can attenuate the lung I/R injury, and mitoKATP plays a vital role in the protective procession of ischemic postconditioning on lung ischemic reperfusion.
