中华创伤杂志
中華創傷雜誌
중화창상잡지
Chinese Journal of Traumatology
2010年
4期
349-353
,共5页
李京%孙善全%刘辉%张兴业%高宝兵
李京%孫善全%劉輝%張興業%高寶兵
리경%손선전%류휘%장흥업%고보병
再灌注损伤%内质网%细胞凋亡%半胱氨酸蛋白酶类
再灌註損傷%內質網%細胞凋亡%半胱氨痠蛋白酶類
재관주손상%내질망%세포조망%반광안산단백매류
Reperfusion injury%Endoplasmic reticulum%Cell apoptosis%Cysteine protein
目的 观察在大鼠脊髓缺血再灌注损伤过程中Ire1α与caspase-12的表达变化规律及其与神经细胞凋亡的关系. 方法 健康成年SD大鼠55只,用随机数字表法分为2组:(1)脊髓压迫缺血再灌注组(手术组,50只大鼠),每个时相点10只,采用自制压迫装置制备脊髓压迫缺血再灌注模型;(2)假手术对照组(手术组,5只大鼠),只做全椎板切除不做脊髓压迫.用TUNEL、免疫组化、Western blot和免疫荧光标记等方法 ,分别于缺血再灌注后1,4,8,16和24 h检测压迫段脊髓组织中细胞凋亡以及lre1α,caspase-12的表达变化情况. 结果 细胞凋亡数量随着缺血再灌注时间的延长而增加.手术组Ire1α、caspase-12的阳性细胞数及蛋白量于再灌注1 h开始增加,16 h达峰值,24 h开始减少,但仍然高于假手术对照组(P<0.05). 结论 Ire1α与caspase-12共同参与了内质网应激介导的神经细胞凋亡.
目的 觀察在大鼠脊髓缺血再灌註損傷過程中Ire1α與caspase-12的錶達變化規律及其與神經細胞凋亡的關繫. 方法 健康成年SD大鼠55隻,用隨機數字錶法分為2組:(1)脊髓壓迫缺血再灌註組(手術組,50隻大鼠),每箇時相點10隻,採用自製壓迫裝置製備脊髓壓迫缺血再灌註模型;(2)假手術對照組(手術組,5隻大鼠),隻做全椎闆切除不做脊髓壓迫.用TUNEL、免疫組化、Western blot和免疫熒光標記等方法 ,分彆于缺血再灌註後1,4,8,16和24 h檢測壓迫段脊髓組織中細胞凋亡以及lre1α,caspase-12的錶達變化情況. 結果 細胞凋亡數量隨著缺血再灌註時間的延長而增加.手術組Ire1α、caspase-12的暘性細胞數及蛋白量于再灌註1 h開始增加,16 h達峰值,24 h開始減少,但仍然高于假手術對照組(P<0.05). 結論 Ire1α與caspase-12共同參與瞭內質網應激介導的神經細胞凋亡.
목적 관찰재대서척수결혈재관주손상과정중Ire1α여caspase-12적표체변화규률급기여신경세포조망적관계. 방법 건강성년SD대서55지,용수궤수자표법분위2조:(1)척수압박결혈재관주조(수술조,50지대서),매개시상점10지,채용자제압박장치제비척수압박결혈재관주모형;(2)가수술대조조(수술조,5지대서),지주전추판절제불주척수압박.용TUNEL、면역조화、Western blot화면역형광표기등방법 ,분별우결혈재관주후1,4,8,16화24 h검측압박단척수조직중세포조망이급lre1α,caspase-12적표체변화정황. 결과 세포조망수량수착결혈재관주시간적연장이증가.수술조Ire1α、caspase-12적양성세포수급단백량우재관주1 h개시증가,16 h체봉치,24 h개시감소,단잉연고우가수술대조조(P<0.05). 결론 Ire1α여caspase-12공동삼여료내질망응격개도적신경세포조망.
Objective To investigate the expression changes of Ire1α and caspase-12 in rats with spinal cord ischemia-reperfusion injury.Methods Fifty-five adult SD rats(250-300 g)were randomly divided into control group(re=5)and operation group(n=50).The spinal cord ischemia-reperfusion models were established and the neuronal apoptosis was detected by terminal deoxynucleotidyl transferasemediated dUTP nick end labeling(TUNEL).The expressions of Ire1α and caspase-12 in spinal cord tissue were detected by immunohistochemistry,immunofluorescence and Western blot analysis at 1,4,8,16and 24 hours after ischemia-reperfusion.Results TUNEL staining showed that the number of apoptotic cells was gradually elevated with time.The expressions of Ire 1α and caspase-12 were increased at 1 hour after reperfusion,and peaked at 16 hours,but began to decline at 24 hours after reperfusion.The number of neurons with positive expressions of Irelaand caspase-12 was significantly higher than that of control group(P<0.05).Conclusion Ire 1α and caspase-12 synergistically participate in the neuronal apoptosis induced by the endoplasmic reticulum stress.