中国医药导报
中國醫藥導報
중국의약도보
CHINA MEDICAL HERALD
2014年
18期
12-16
,共5页
叶博%张国荣%黄俊梅%尹哲%陶磊
葉博%張國榮%黃俊梅%尹哲%陶磊
협박%장국영%황준매%윤철%도뢰
加速度%低压低氧%大鼠%心肌损伤%抗氧化%一氧化氮
加速度%低壓低氧%大鼠%心肌損傷%抗氧化%一氧化氮
가속도%저압저양%대서%심기손상%항양화%일양화담
Acceleration%Hypobaric hypoxia%Rats%Myocardial injuries%Anti-oxidant%NO
目的：从心肌抗氧化系统及一氧化氮(NO)代谢通路研究低压低氧预处理对加速度环境下心肌细胞病理生理变化的影响,解释航空加速度环境下心肌组织的损伤机制,探讨低压低氧预处理的保护机制.方法24只雄性SD大鼠随机分为3组(n=8),C组为空白对照组,HHP+10 Gz组为5000 m高空低压低氧预处理4 h/d连续4 d后暴露10 Gz加速度组,10 Gz组为直接暴露10 Gz加速度组,各组按上述处理后,取大鼠心肌组织,委托北京华英生物技术研究室检测超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-PX)、谷胱甘肽(GSH)、丙二醛(MDA)、热休克蛋白-70(HSP-70)以及一氧化氮(NO)、亚硝酸盐(NO2-)、硝酸盐(NO3-)、内皮型一氧化氮合酶(eNOS)、诱导型一氧化氮合酶(iNOS)、神经型一氧化氮合酶(nNOS)的变化.结果 SOD水平院C组[(8.242±1.562)U/mg]和HHP+10 Gz组[(7.660±1.208)U/mg]高于10 Gz组[(4.773±0.665)U/mg],差异均有统计学意义(均P<0.05)；CAT水平院C组[(2.348±0.382)U/mg]高于HHP+10 Gz组[(1.955±0.204)U/mg]和10 Gz组[(1.749±0.165)U/mg],HHP+10 Gz组高于10Gz组,差异均有统计学意义(均P<0.05)；GSH-PX水平院C组[(91.864±38.788)U/mg]高于10 Gz组[(47.821±8.208)U/mg],差异有统计学意义(P<0.05)；GSH水平院C组[(0.748±0.182)μmol/g]和HHP+10 Gz组[(0.593±0.205)μmol/g]高于10 Gz组[(0.232±0.034)μmol/g],差异均有统计学意义(均P<0.05)；MDA水平院各组间差异无统计学意义(P>0.054)；HSP-70水平院C组[(1.415±0.500)ng/mg]低于HHP+10 Gz组[(2.189±0.659)ng/mg]和10 Gz组[(2.452±0.926)ng/mg],差异均有统计学意义(均P<0.05)；NO水平院C组[(1.932±0.496)μmol/g]低于HHP+10 Gz组[(2.751±0.784)μmol/g]和10 Gz组[(3.185±0.769)μmol/g],差异均有统计学意义(均P<0.05)；NO2-水平院C组[(1.277±0.279)μmol/g]低于HHP+10 Gz组[(1.800±0.568)μmol/g]和10 Gz组[(1.970±0.362)μmol/g],差异均有统计学意义(均P<0.05)；NO3-水平院C组[(2.191±0.426)μmol/g]低于HHP+10Gz组[(2.898±0.500)μmol/g]和10 Gz组[(2.995±0.445)μmol/g],差异均有统计学意义(均 P <0.05)；eNOS水平院C组[(3.726±0.498)U/mg]低于HHP+10 Gz组[(5.081±0.994)U/mg]和10 Gz组[(5.937±1.423)U/mg],差异均有统计学意义(均P<0.05)；iNOS水平院C组[(3.668±0.379)U/mg]低于HHP+10 Gz组[(4.382±0.567)U/mg]和10 Gz组[(4.986±1.318)U/mg],差异均有统计学意义(均P<0.05)；nNOS水平院C组[(0.830±0.117)U/mg]低于HHP+10 Gz组[(1.044±0.190)U/mg]和10 Gz组[(1.226±0.300)U/mg],差异均有统计学意义(均P<0.05).结论低压低氧预处理可以降低加速度对心肌造成的氧化损伤,对心肌具有保护作用,其机制与低压低氧预处理增强了大鼠体内抗氧化酶活性,减轻氧化应激对NOS的激活从而抑制NO的大量释放有关。
目的：從心肌抗氧化繫統及一氧化氮(NO)代謝通路研究低壓低氧預處理對加速度環境下心肌細胞病理生理變化的影響,解釋航空加速度環境下心肌組織的損傷機製,探討低壓低氧預處理的保護機製.方法24隻雄性SD大鼠隨機分為3組(n=8),C組為空白對照組,HHP+10 Gz組為5000 m高空低壓低氧預處理4 h/d連續4 d後暴露10 Gz加速度組,10 Gz組為直接暴露10 Gz加速度組,各組按上述處理後,取大鼠心肌組織,委託北京華英生物技術研究室檢測超氧化物歧化酶(SOD)、過氧化氫酶(CAT)、穀胱甘肽過氧化物酶(GSH-PX)、穀胱甘肽(GSH)、丙二醛(MDA)、熱休剋蛋白-70(HSP-70)以及一氧化氮(NO)、亞硝痠鹽(NO2-)、硝痠鹽(NO3-)、內皮型一氧化氮閤酶(eNOS)、誘導型一氧化氮閤酶(iNOS)、神經型一氧化氮閤酶(nNOS)的變化.結果 SOD水平院C組[(8.242±1.562)U/mg]和HHP+10 Gz組[(7.660±1.208)U/mg]高于10 Gz組[(4.773±0.665)U/mg],差異均有統計學意義(均P<0.05)；CAT水平院C組[(2.348±0.382)U/mg]高于HHP+10 Gz組[(1.955±0.204)U/mg]和10 Gz組[(1.749±0.165)U/mg],HHP+10 Gz組高于10Gz組,差異均有統計學意義(均P<0.05)；GSH-PX水平院C組[(91.864±38.788)U/mg]高于10 Gz組[(47.821±8.208)U/mg],差異有統計學意義(P<0.05)；GSH水平院C組[(0.748±0.182)μmol/g]和HHP+10 Gz組[(0.593±0.205)μmol/g]高于10 Gz組[(0.232±0.034)μmol/g],差異均有統計學意義(均P<0.05)；MDA水平院各組間差異無統計學意義(P>0.054)；HSP-70水平院C組[(1.415±0.500)ng/mg]低于HHP+10 Gz組[(2.189±0.659)ng/mg]和10 Gz組[(2.452±0.926)ng/mg],差異均有統計學意義(均P<0.05)；NO水平院C組[(1.932±0.496)μmol/g]低于HHP+10 Gz組[(2.751±0.784)μmol/g]和10 Gz組[(3.185±0.769)μmol/g],差異均有統計學意義(均P<0.05)；NO2-水平院C組[(1.277±0.279)μmol/g]低于HHP+10 Gz組[(1.800±0.568)μmol/g]和10 Gz組[(1.970±0.362)μmol/g],差異均有統計學意義(均P<0.05)；NO3-水平院C組[(2.191±0.426)μmol/g]低于HHP+10Gz組[(2.898±0.500)μmol/g]和10 Gz組[(2.995±0.445)μmol/g],差異均有統計學意義(均 P <0.05)；eNOS水平院C組[(3.726±0.498)U/mg]低于HHP+10 Gz組[(5.081±0.994)U/mg]和10 Gz組[(5.937±1.423)U/mg],差異均有統計學意義(均P<0.05)；iNOS水平院C組[(3.668±0.379)U/mg]低于HHP+10 Gz組[(4.382±0.567)U/mg]和10 Gz組[(4.986±1.318)U/mg],差異均有統計學意義(均P<0.05)；nNOS水平院C組[(0.830±0.117)U/mg]低于HHP+10 Gz組[(1.044±0.190)U/mg]和10 Gz組[(1.226±0.300)U/mg],差異均有統計學意義(均P<0.05).結論低壓低氧預處理可以降低加速度對心肌造成的氧化損傷,對心肌具有保護作用,其機製與低壓低氧預處理增彊瞭大鼠體內抗氧化酶活性,減輕氧化應激對NOS的激活從而抑製NO的大量釋放有關。
목적：종심기항양화계통급일양화담(NO)대사통로연구저압저양예처리대가속도배경하심기세포병리생리변화적영향,해석항공가속도배경하심기조직적손상궤제,탐토저압저양예처리적보호궤제.방법24지웅성SD대서수궤분위3조(n=8),C조위공백대조조,HHP+10 Gz조위5000 m고공저압저양예처리4 h/d련속4 d후폭로10 Gz가속도조,10 Gz조위직접폭로10 Gz가속도조,각조안상술처리후,취대서심기조직,위탁북경화영생물기술연구실검측초양화물기화매(SOD)、과양화경매(CAT)、곡광감태과양화물매(GSH-PX)、곡광감태(GSH)、병이철(MDA)、열휴극단백-70(HSP-70)이급일양화담(NO)、아초산염(NO2-)、초산염(NO3-)、내피형일양화담합매(eNOS)、유도형일양화담합매(iNOS)、신경형일양화담합매(nNOS)적변화.결과 SOD수평원C조[(8.242±1.562)U/mg]화HHP+10 Gz조[(7.660±1.208)U/mg]고우10 Gz조[(4.773±0.665)U/mg],차이균유통계학의의(균P<0.05)；CAT수평원C조[(2.348±0.382)U/mg]고우HHP+10 Gz조[(1.955±0.204)U/mg]화10 Gz조[(1.749±0.165)U/mg],HHP+10 Gz조고우10Gz조,차이균유통계학의의(균P<0.05)；GSH-PX수평원C조[(91.864±38.788)U/mg]고우10 Gz조[(47.821±8.208)U/mg],차이유통계학의의(P<0.05)；GSH수평원C조[(0.748±0.182)μmol/g]화HHP+10 Gz조[(0.593±0.205)μmol/g]고우10 Gz조[(0.232±0.034)μmol/g],차이균유통계학의의(균P<0.05)；MDA수평원각조간차이무통계학의의(P>0.054)；HSP-70수평원C조[(1.415±0.500)ng/mg]저우HHP+10 Gz조[(2.189±0.659)ng/mg]화10 Gz조[(2.452±0.926)ng/mg],차이균유통계학의의(균P<0.05)；NO수평원C조[(1.932±0.496)μmol/g]저우HHP+10 Gz조[(2.751±0.784)μmol/g]화10 Gz조[(3.185±0.769)μmol/g],차이균유통계학의의(균P<0.05)；NO2-수평원C조[(1.277±0.279)μmol/g]저우HHP+10 Gz조[(1.800±0.568)μmol/g]화10 Gz조[(1.970±0.362)μmol/g],차이균유통계학의의(균P<0.05)；NO3-수평원C조[(2.191±0.426)μmol/g]저우HHP+10Gz조[(2.898±0.500)μmol/g]화10 Gz조[(2.995±0.445)μmol/g],차이균유통계학의의(균 P <0.05)；eNOS수평원C조[(3.726±0.498)U/mg]저우HHP+10 Gz조[(5.081±0.994)U/mg]화10 Gz조[(5.937±1.423)U/mg],차이균유통계학의의(균P<0.05)；iNOS수평원C조[(3.668±0.379)U/mg]저우HHP+10 Gz조[(4.382±0.567)U/mg]화10 Gz조[(4.986±1.318)U/mg],차이균유통계학의의(균P<0.05)；nNOS수평원C조[(0.830±0.117)U/mg]저우HHP+10 Gz조[(1.044±0.190)U/mg]화10 Gz조[(1.226±0.300)U/mg],차이균유통계학의의(균P<0.05).결론저압저양예처리가이강저가속도대심기조성적양화손상,대심기구유보호작용,기궤제여저압저양예처리증강료대서체내항양화매활성,감경양화응격대NOS적격활종이억제NO적대량석방유관。
Objective To evaluate the effect of hypobaric hypoxia preconditioning (HHP) on myocardial cells pathological physiology changes under acceleration environment from myocardial antioxidant system and NO metabolic pathways. To explain the mechanism of myocardial tissue damage by acceleration environment, explore the protection mechanism of HHP. Methods 24 male SD rats were randomly divided into 3 groups (n=8), C group was the blank control group, HHP+10 Gz group was 5000 m altitude hypoxic preconditioning 4 h/d for 4 days then exposure to 10 Gz acceleration, 10 Gz group was directly exposed to 10 Gz acceleration. After the treatment above, SOD, CAT, GSH-PX, GSH, MDA, HSP-70 and NO, NO2-, NO3-, eNOS, iNOS, nNOS content of the cardiac muscle tissue of rats were determined by Beijing Huaying Biotechnology Research Company. Results SOD level: group C [(8.242±1.562) U/mg] was higher than group 10 Gz [(4.773±0.665) U/mg], group HHP+10 Gz [(7.660±1.208) U/mg] was higher than group 10 Gz, the differences were statistically significant (P<0.05). CAT level:group C [(2.348±0.382) U/mg] was higher than group HHP+10 Gz [(1.955±0.204) U/mg] and group 10 Gz [(1.749±0.165) U/mg], group HHP+10 Gz was higher than group 10Gz, the differences were statistically significant (P< 0.05). GSH-PX level: group C [(91.864±38.788) U/mg] was higher than group 10 Gz [(47.821±8.208) U/mg] , the differencs was statistically significant (P< 0.05). GSH level:group C [(0.748±0.182) μmol/g] and group HHP+10 Gz [(0.593±0.205) μmol/g] were higher than group 10 Gz [(0.232±0.034) μmol/g], the differences were statistically significant (P< 0.05). MDA level: there was no statistically significant differences (P>0.05). HSP-70 levls: group C [(1.415±0.500) ng/mg] was lower than group HHP+10 Gz [(2.189±0.659) ng/mg] and group 10 Gz [(2.452±0.926) ng/mg], the differences were statistically significant (P<0.05). NO level: group C [(1.932±0.496) μmol/g] was lower than group HHP+10 Gz [(2.751±0.784) μmol/g] and group 10 Gz [(3.185±0.769)μmol/g], the differences were statistically significant (P< 0.05). NO2-level: group C [(1.277±0.279) μmol/g] was lower than group HHP+10 Gz [(1.800±0.568) μmol/g] and group 10 Gz [(1.970±0.362) μmol/g], the differences were statistically significant (P < 0.05). NO3- level: group C [(2.191±0.426) μmol/g] was lower than group HHP+10 Gz [(2.898±0.500) μmol/g] and group 10 Gz [(2.995±0.445) μmol/g], the differences were statistically significant (P <0.05). eNOS level:group C [(3.726±0.498) U/mg] was lower than group HHP+10 Gz [(5.081±0.994) U/mg] and group 10 Gz [(5.937±1.423) U/mg], the differences were statistically significant (P<0.05). iNOS level: group C [(3.668±0.379) U/mg] was lower than group HHP+10 Gz [(4.382±0.567) U/mg] and group 10 Gz [(4.986±1.318) U/mg], the differences were statistically significant (P<0.05). nNOS level:group C [(0.830±0.117) U/mg] was lower than group HHP+10 Gz [(1.044±0.190) U/mg] and group 10 Gz [(1.226±0.300) U/mg], the differences were statistically significant (P< 0.05). Conclusion HHP can reduce oxidative damage of myocardial tissue caused by acceleration and has myocardial protective effect, the mechanism is related to enhancing the activity of antioxidant enzymes and reducing oxidative stress on the activation of NOS and then inhibiting the release of NO in rats.
