中华实用儿科临床杂志
中華實用兒科臨床雜誌
중화실용인과림상잡지
Journal of Applied Clinical Pediatrics
2015年
11期
860-862
,共3页
吕娟娟%陈志江%郑贵浪%王斌%陶少华%项丹%谢美燕%刘翠%黄锦达
呂娟娟%陳誌江%鄭貴浪%王斌%陶少華%項丹%謝美燕%劉翠%黃錦達
려연연%진지강%정귀랑%왕빈%도소화%항단%사미연%류취%황금체
脓毒症相关性脑病%线粒体功能障碍%氧化应激%远期损伤
膿毒癥相關性腦病%線粒體功能障礙%氧化應激%遠期損傷
농독증상관성뇌병%선립체공능장애%양화응격%원기손상
Sepsis-associated encephalopathy%Mitochondrial dysfunction%Oxidative stress%Long-term injury
目的 探讨脓毒症相关性脑病(SAE)远期脑线粒体损伤与氧化应激的关系.方法 通过腹腔注射革兰阴性菌脂多糖(LPS)建立脓毒症模型.出现SAE症状的大鼠(SAE组)及对照组大鼠分别在相应时间点进行神经反射评估后处死,取脑组织提取线粒体.通过流式细胞仪检测线粒体膜电位(MMP)及活性氧(ROS),通过酶标仪检测超氧化物歧化酶(SOD)、丙二醛(MDA)、诱导型一氧化氮合成酶(iNOS)和一氧化氮(NO)水平.结果 神经反射评估在12 h已经开始下降,并缓慢恢复.MMP在腹腔注射LPS后明显下降,48 h降至最低,差异有统计学意义(F=75.785,P＜0.05),72 h部分恢复;ROS 48 h明显升高伴随SOD的明显下降,差异均有统计学意义(F=111.274,21.808,P均＜0.05),72 h部分恢复;MDA、iNOS和NO 48 h增加达到峰值,差异均有统计学意义(F=21.955、61.076、21.184,P均＜0.05),72 h部分恢复.脓毒症大鼠脑组织线粒体SOD活性与MMP呈强正相关关系(r=0.856,P＜0.05);脓毒症大鼠脑组织线粒体ROS水平、MDA水平、iNOS活性和NO水平与MMP呈强负相关关系(r=-0.852、-0.890、-0.940、-0.794,P均＜0.05).结论 在SAE模型中,脑线粒体损伤的高峰可能发生在48 h左右,氧化应激的明显增强可能是导致远期线粒体功能障碍的原因之一.
目的 探討膿毒癥相關性腦病(SAE)遠期腦線粒體損傷與氧化應激的關繫.方法 通過腹腔註射革蘭陰性菌脂多糖(LPS)建立膿毒癥模型.齣現SAE癥狀的大鼠(SAE組)及對照組大鼠分彆在相應時間點進行神經反射評估後處死,取腦組織提取線粒體.通過流式細胞儀檢測線粒體膜電位(MMP)及活性氧(ROS),通過酶標儀檢測超氧化物歧化酶(SOD)、丙二醛(MDA)、誘導型一氧化氮閤成酶(iNOS)和一氧化氮(NO)水平.結果 神經反射評估在12 h已經開始下降,併緩慢恢複.MMP在腹腔註射LPS後明顯下降,48 h降至最低,差異有統計學意義(F=75.785,P＜0.05),72 h部分恢複;ROS 48 h明顯升高伴隨SOD的明顯下降,差異均有統計學意義(F=111.274,21.808,P均＜0.05),72 h部分恢複;MDA、iNOS和NO 48 h增加達到峰值,差異均有統計學意義(F=21.955、61.076、21.184,P均＜0.05),72 h部分恢複.膿毒癥大鼠腦組織線粒體SOD活性與MMP呈彊正相關關繫(r=0.856,P＜0.05);膿毒癥大鼠腦組織線粒體ROS水平、MDA水平、iNOS活性和NO水平與MMP呈彊負相關關繫(r=-0.852、-0.890、-0.940、-0.794,P均＜0.05).結論 在SAE模型中,腦線粒體損傷的高峰可能髮生在48 h左右,氧化應激的明顯增彊可能是導緻遠期線粒體功能障礙的原因之一.
목적 탐토농독증상관성뇌병(SAE)원기뇌선립체손상여양화응격적관계.방법 통과복강주사혁란음성균지다당(LPS)건립농독증모형.출현SAE증상적대서(SAE조)급대조조대서분별재상응시간점진행신경반사평고후처사,취뇌조직제취선립체.통과류식세포의검측선립체막전위(MMP)급활성양(ROS),통과매표의검측초양화물기화매(SOD)、병이철(MDA)、유도형일양화담합성매(iNOS)화일양화담(NO)수평.결과 신경반사평고재12 h이경개시하강,병완만회복.MMP재복강주사LPS후명현하강,48 h강지최저,차이유통계학의의(F=75.785,P＜0.05),72 h부분회복;ROS 48 h명현승고반수SOD적명현하강,차이균유통계학의의(F=111.274,21.808,P균＜0.05),72 h부분회복;MDA、iNOS화NO 48 h증가체도봉치,차이균유통계학의의(F=21.955、61.076、21.184,P균＜0.05),72 h부분회복.농독증대서뇌조직선립체SOD활성여MMP정강정상관관계(r=0.856,P＜0.05);농독증대서뇌조직선립체ROS수평、MDA수평、iNOS활성화NO수평여MMP정강부상관관계(r=-0.852、-0.890、-0.940、-0.794,P균＜0.05).결론 재SAE모형중,뇌선립체손상적고봉가능발생재48 h좌우,양화응격적명현증강가능시도치원기선립체공능장애적원인지일.
Objective To investigate the long-term mitochondrial dysfunction and oxidative stress in a sepsis-associated encephalopathy(SAE) model.Methods To initiate experimental sepsis,male Wistar rats were injected intraperitoneally with 10 mg/kg of lipopolysaccharide (LPS) dissolved in sodium chloride.Animals were evaluated by neurologic reflex scores before sacrifice and brain tissues were quickly removed at the indicated time points (0 h for control group and 12,24,48,72 h post injections for SAE groups).Cerebral mitochondrial membrane potential (MMP) and reactive oxygen species(ROS) were detected by flow cytometer and superoxide dismutase(SOD),malondialdehyde (MDA),inducible nitric oxide synthase (iNOS) and nitric oxide (NO) were determined by using microplate reader.Results Deteriorated neurological reflexes were found since 12 h and recovered slowly.Cerebral MMP in 12 h SAE group was decreased significantly compared with that in the control group.MMP was decreased to the lowest level at 48 h (F =75.785,P ＜0.05),and partly recovered at 72 h.ROS,MDA,iNOS and NO were increased significantly at 48 h (F =111.274,21.955,61.076,21.184,all P ＜ 0.05) and partly recovered at 72 h.SOD changed controversially with ROS (F =21.808,P ＜ 0.05).SOD showed strong positive linear correlations with M MP (r =0.856,P ＜ 0.05),whereas ROS,MDA,iNOS and NO showed strong negative linear correlations with MMP (r =-0.852,-0.890,-0.940,-0.794,all P ＜ 0.05).Conclusions These results suggest that long-term brain mitochondrial dysfunction of lipopolysaccharide-induced septic rat is partly affected due to an increase in oxidative stress and has a turning-point near 48 h post injections.
