中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2012年
11期
2033-2038
,共6页
李兴国%郑宏宇%李文%李宏昆%赵学凌%王兵%吴雪梅
李興國%鄭宏宇%李文%李宏昆%趙學凌%王兵%吳雪梅
리흥국%정굉우%리문%리굉곤%조학릉%왕병%오설매
氧化应激%丙二醛%总超氧化物岐化酶%谷胱甘肽还原酶%Rac1/2%深静脉血栓%组织构建
氧化應激%丙二醛%總超氧化物岐化酶%穀胱甘肽還原酶%Rac1/2%深靜脈血栓%組織構建
양화응격%병이철%총초양화물기화매%곡광감태환원매%Rac1/2%심정맥혈전%조직구건
背景:深静脉血栓形成的分子机制及核心调控网络目前仍未完全阐明.目的:观察氧化应激和Rac1/2 在大鼠创伤性深静脉血栓形成中的作用.方法:将SD 大鼠采用股静脉钳夹联合下肢石膏制动构建大鼠深静脉血栓模型.不同时间点(造模后2.5 h 和25 h)解剖股静脉观测血栓的发生率及严重程度.再将模型大鼠分为:血栓形成前组(造模后2.5 h)、血栓形成组(创伤后25 h)、血栓未形成组(造模后25 h).获取股静脉壁组织,提取总蛋白质和总RNA.结果与结论:比色法检测结果显示,相比血栓未形成组,血栓形成组大鼠股静脉组织中丙二醛的含量最高(P < 0.05),血栓形成前组次之(P < 0.05);而总超氧化物岐化酶、谷胱甘肽还原酶的活性在血栓形成组最低,血栓形成前组次之(P < 0.05).基因芯片分析及real-time PCR 结果发现,相比血栓未形成组,血栓形成组大鼠股静脉组织中Rac1 和Rac2 的表达最高(P < 0.05),血栓形成前组次之(P < 0.05).结果证实,局部静脉血管壁组织中丙二醛,Rac1/2 表达上调,总超氧化物岐化酶和谷胱甘肽还原酶活性降低,可能导致创伤性深静脉血栓的形成.
揹景:深靜脈血栓形成的分子機製及覈心調控網絡目前仍未完全闡明.目的:觀察氧化應激和Rac1/2 在大鼠創傷性深靜脈血栓形成中的作用.方法:將SD 大鼠採用股靜脈鉗夾聯閤下肢石膏製動構建大鼠深靜脈血栓模型.不同時間點(造模後2.5 h 和25 h)解剖股靜脈觀測血栓的髮生率及嚴重程度.再將模型大鼠分為:血栓形成前組(造模後2.5 h)、血栓形成組(創傷後25 h)、血栓未形成組(造模後25 h).穫取股靜脈壁組織,提取總蛋白質和總RNA.結果與結論:比色法檢測結果顯示,相比血栓未形成組,血栓形成組大鼠股靜脈組織中丙二醛的含量最高(P < 0.05),血栓形成前組次之(P < 0.05);而總超氧化物岐化酶、穀胱甘肽還原酶的活性在血栓形成組最低,血栓形成前組次之(P < 0.05).基因芯片分析及real-time PCR 結果髮現,相比血栓未形成組,血栓形成組大鼠股靜脈組織中Rac1 和Rac2 的錶達最高(P < 0.05),血栓形成前組次之(P < 0.05).結果證實,跼部靜脈血管壁組織中丙二醛,Rac1/2 錶達上調,總超氧化物岐化酶和穀胱甘肽還原酶活性降低,可能導緻創傷性深靜脈血栓的形成.
배경:심정맥혈전형성적분자궤제급핵심조공망락목전잉미완전천명.목적:관찰양화응격화Rac1/2 재대서창상성심정맥혈전형성중적작용.방법:장SD 대서채용고정맥겸협연합하지석고제동구건대서심정맥혈전모형.불동시간점(조모후2.5 h 화25 h)해부고정맥관측혈전적발생솔급엄중정도.재장모형대서분위:혈전형성전조(조모후2.5 h)、혈전형성조(창상후25 h)、혈전미형성조(조모후25 h).획취고정맥벽조직,제취총단백질화총RNA.결과여결론:비색법검측결과현시,상비혈전미형성조,혈전형성조대서고정맥조직중병이철적함량최고(P < 0.05),혈전형성전조차지(P < 0.05);이총초양화물기화매、곡광감태환원매적활성재혈전형성조최저,혈전형성전조차지(P < 0.05).기인심편분석급real-time PCR 결과발현,상비혈전미형성조,혈전형성조대서고정맥조직중Rac1 화Rac2 적표체최고(P < 0.05),혈전형성전조차지(P < 0.05).결과증실,국부정맥혈관벽조직중병이철,Rac1/2 표체상조,총초양화물기화매화곡광감태환원매활성강저,가능도치창상성심정맥혈전적형성.
BACKGROUND: The molecular mechanism and core regulatory network of deep vein thrombosis are not fully clarified yet.OBJECTIVE: To explore the roles of oxidative stress and Rac1/2 in rat deep vein thrombosis.METHODS: Deep vein thrombosis model in SD rats was established by a champing method femoral veins clamping combinedwith fixation of the lower extremity with plaster. The incidence and serious degree of thrombus were observed by dissecting ratfemoral vein at different time points (2.5 and 25 hours after modeling). The model rats were divided into pre-thrombogenesisgroup (2.5 hours after modeling), thrombogenesis group (25 hours after modeling) and non-thrombogenesis group (25 hours aftermodeling). Then total RNA and protein were extracted from the femoral venous wall tissues.RESULTS AND CONCLUSION: Colorimetry results showed that compared with the non-thrombogenesis group, theconcentration of malondiadehyde in rat femoral vein wall tissues of the thrombogenesis group was the highest (P < 0.05), followedby that of the pre-thrombogenesis group (P < 0.05). The concentrations of total superoxide dismutase and glutathione reductasein the thrombogenesis group were the lowest, followed by those in the pre-thrombogenesis group (P < 0.05). The results of genechip hybridization analysis and real-time PCR showed that compared with the non-thrombogenesis group, the expressions ofRac1 and Rac2 in rat femoral vein wall tissues of thrombogenesis group increased the most, followed by that of thepre-thrombogenesis group (P < 0.05). These findings indicate that the up-regulation of malondialdehyde and Rac1/2 as well asthe activity decrease of total superoxide dismutase and glutathione reductase may lead to the formation of deep venousthrombosis.