CAJ | 학술논문

目的研究早产儿氧暴露后体内活性氧簇产生可能的线粒体氧化应激信号传导途径.方法选择2012年7月至12月胎龄为34周以下在泸州医学院附属医院新生儿科住院诊断为呼吸衰竭需给氧支持治疗的早产儿20例作为高体积分数氧(高氧)组(吸氧体积分数＞400 mL/L,吸氧时间48～69 h),相同时间段置于同一室未用氧的早产儿20例作为对照组,未发生呼吸衰竭,暴露于空气时间＞48 h.用免疫组织化学方法检测高氧组和对照组早产儿外周血单个核细胞内蛋白激酶C-β(PKCβ)、衔接蛋白(p66Shc)、脯氨酰异构酶(Pin1)和胞质磷酸化p66Shc-Ser36蛋白的表达及用荧光显微镜技术检测线粒体活性氧的产生.结果与对照组相比,高氧组外周血单个核细胞内PKCβ、p66Shc、Pin1和磷酸化p66Shc-Ser36蛋白表达增加及活性氧产生增加,差异均具有统计学意义(t =21.139、5.592、7.476、16.895、10.586,P均＜0.001),且高氧组活性氧的产生与PKCβ、p66Shc、Pinl和磷酸化p66Shc Ser36蛋白表达呈正相关关系(r=0.893、0.795、0.681、0.663,P均＜0.001).结论 PKCβ/p66Shc氧化应激信号通路可能介导早产儿氧暴露后体内活性氧簇的产生.
목적 연구조산인양폭로후체내활성양족산생가능적선립체양화응격신호전도도경.방법 선택2012년7월지12월태령위34주이하재로주의학원부속의원신생인과주원진단위호흡쇠갈수급양지지치료적조산인20례작위고체적분수양(고양)조(흡양체적분수＞400 mL/L,흡양시간48～69 h),상동시간단치우동일실미용양적조산인20례작위대조조,미발생호흡쇠갈,폭로우공기시간＞48 h.용면역조직화학방법검측고양조화대조조조산인외주혈단개핵세포내단백격매C-β(PKCβ)、함접단백(p66Shc)、포안선이구매(Pin1)화포질린산화p66Shc-Ser36단백적표체급용형광현미경기술검측선립체활성양적산생.결과 여대조조상비,고양조외주혈단개핵세포내PKCβ、p66Shc、Pin1화린산화p66Shc-Ser36단백표체증가급활성양산생증가,차이균구유통계학의의(t =21.139、5.592、7.476、16.895、10.586,P균＜0.001),차고양조활성양적산생여PKCβ、p66Shc、Pinl화린산화p66Shc Ser36단백표체정정상관관계(r=0.893、0.795、0.681、0.663,P균＜0.001).결론 PKCβ/p66Shc양화응격신호통로가능개도조산인양폭로후체내활성양족적산생.
Objective To study the possible mitochondria oxidative stress signal transduction pathway,which probably mediates the production of reactive oxygen species in premature infants exposed to hyperoxia.Methods Hyperoxia group:20 cases of premature infants whose gestational age was below 34 weeks were diagnosed as respiratory failure (treated with exposed to over 400 mL/L oxygen 48-69 h) in Department of Neonatology,the Affiliated Hospital of Luzhou Medical College,from Jul.to Dec.2012.Control group:20 cases of premature infants with the same gestational age were diagnosed as no respiratory failure(exposed to air over 48 h in the same room simultaneously).The expression of protein kinase C-beta (PKC β)/the 66-kDa isoform of the growth factor adaptor Shc (p66Shc)/prolyl isomerase 1 (Pin1)/phosphorylated the 66-kDa isoform of the growth factor adaptor Shc-Ser36 (p66Shc-Ser36) were detected by immunohistochemistry and the production of mitochondrial reactive oxygen was detected by fluorescence microscope in the peripheral blood mononuclear cell of hyperoxia group and control group.Results Compared with the control group,the expressions of PKCβ,p66Shc,Pin1,phosphorylated p66Shc-Ser36 and the production of reactive oxygen in hyperoxia group were significantly increased (t =21.139,5.592,7.476,16.895,10.586,all P ＜ 0.001).There were positive correlations between the production of reactive oxygen and the expressions of PKCβ,p66Shc,Pin1,phosphorylated p66Shc-Ser36 in hyperoxia group(r =0.893,0.795,0.681,0.663,all P ＜ 0.001).Conclusion PKCβ/p66Shc oxidative stress pathway might mediate the production of reactive oxygen species in premature infants exposed to hyperoxia.