中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
18期
2879-2883
,共5页
张颖%张海峰%任青爱%谢晓华
張穎%張海峰%任青愛%謝曉華
장영%장해봉%임청애%사효화
实验动物%消化系统损伤模型%硫化氢%肝损害%创伤%线粒体%截肢%脂质过氧化%炎症反应
實驗動物%消化繫統損傷模型%硫化氫%肝損害%創傷%線粒體%截肢%脂質過氧化%炎癥反應
실험동물%소화계통손상모형%류화경%간손해%창상%선립체%절지%지질과양화%염증반응
Hydrogen Sulfide%Amputation%Liver%Mitochondria
背景:截肢是一种特殊类型的创伤,创伤导致肝脏损害的机制及硫化氢对肝脏的作用目前尚不明确。目的:探索构建截肢创伤模型大鼠的肝脏损伤,以硫化氢(H 2 S)对其的影响。<br> 方法:将Wistar大鼠和SD大鼠分别随机等分为正常组、截肢后6,12,24,72 h组、硫氢化钠(NaHS)组、炔丙基甘氨酸组和为正常组、截肢后6 h组、NaHS组、炔丙基甘氨酸组。除正常组外所有大鼠完全截断左侧于膝关节上方1.2-1.4 cm处结构,并在结扎血管后剪断左侧股静、动脉,建立左后肢的截肢模型大鼠。NaHS组及炔丙基甘氨酸组大鼠分别于截肢后即刻腹腔注射28μmol/kg NaHS和50 mg/kg炔丙基甘氨酸。<br> 结果与结论:与正常组相比,截肢后6h组大鼠肝脏和线粒体结构出现了损伤性改变,血浆及肝脏髓过氧化物酶、丙二醛、H2S/胱硫醚γ-裂解酶水平、血浆及肝脏髓过氧化物酶、丙二醛、肝脏线粒体呼吸控制率、膜电位及ATP酶活性明显降低(P<0.05),NaHS干预后H 2 S/胱硫醚γ-裂解酶水平及以上指标明显升高(P<0.05),但血浆转氨酶并未明显变化(P>0.05)。应用炔丙基甘氨酸后,以上除线粒体指标无明显变化外,多表现为进一步降低,转氨酶也明显下降(P<0.05)。说明H 2 S可减轻截肢模型大鼠肝脏组织脂质过氧化、炎症反应,并使线粒体功能明显改善,但并未减轻肝脏功能的受损。
揹景:截肢是一種特殊類型的創傷,創傷導緻肝髒損害的機製及硫化氫對肝髒的作用目前尚不明確。目的:探索構建截肢創傷模型大鼠的肝髒損傷,以硫化氫(H 2 S)對其的影響。<br> 方法:將Wistar大鼠和SD大鼠分彆隨機等分為正常組、截肢後6,12,24,72 h組、硫氫化鈉(NaHS)組、炔丙基甘氨痠組和為正常組、截肢後6 h組、NaHS組、炔丙基甘氨痠組。除正常組外所有大鼠完全截斷左側于膝關節上方1.2-1.4 cm處結構,併在結扎血管後剪斷左側股靜、動脈,建立左後肢的截肢模型大鼠。NaHS組及炔丙基甘氨痠組大鼠分彆于截肢後即刻腹腔註射28μmol/kg NaHS和50 mg/kg炔丙基甘氨痠。<br> 結果與結論:與正常組相比,截肢後6h組大鼠肝髒和線粒體結構齣現瞭損傷性改變,血漿及肝髒髓過氧化物酶、丙二醛、H2S/胱硫醚γ-裂解酶水平、血漿及肝髒髓過氧化物酶、丙二醛、肝髒線粒體呼吸控製率、膜電位及ATP酶活性明顯降低(P<0.05),NaHS榦預後H 2 S/胱硫醚γ-裂解酶水平及以上指標明顯升高(P<0.05),但血漿轉氨酶併未明顯變化(P>0.05)。應用炔丙基甘氨痠後,以上除線粒體指標無明顯變化外,多錶現為進一步降低,轉氨酶也明顯下降(P<0.05)。說明H 2 S可減輕截肢模型大鼠肝髒組織脂質過氧化、炎癥反應,併使線粒體功能明顯改善,但併未減輕肝髒功能的受損。
배경:절지시일충특수류형적창상,창상도치간장손해적궤제급류화경대간장적작용목전상불명학。목적:탐색구건절지창상모형대서적간장손상,이류화경(H 2 S)대기적영향。<br> 방법:장Wistar대서화SD대서분별수궤등분위정상조、절지후6,12,24,72 h조、류경화납(NaHS)조、결병기감안산조화위정상조、절지후6 h조、NaHS조、결병기감안산조。제정상조외소유대서완전절단좌측우슬관절상방1.2-1.4 cm처결구,병재결찰혈관후전단좌측고정、동맥,건립좌후지적절지모형대서。NaHS조급결병기감안산조대서분별우절지후즉각복강주사28μmol/kg NaHS화50 mg/kg결병기감안산。<br> 결과여결론:여정상조상비,절지후6h조대서간장화선립체결구출현료손상성개변,혈장급간장수과양화물매、병이철、H2S/광류미γ-렬해매수평、혈장급간장수과양화물매、병이철、간장선립체호흡공제솔、막전위급ATP매활성명현강저(P<0.05),NaHS간예후H 2 S/광류미γ-렬해매수평급이상지표명현승고(P<0.05),단혈장전안매병미명현변화(P>0.05)。응용결병기감안산후,이상제선립체지표무명현변화외,다표현위진일보강저,전안매야명현하강(P<0.05)。설명H 2 S가감경절지모형대서간장조직지질과양화、염증반응,병사선립체공능명현개선,단병미감경간장공능적수손。
BACKGROUND:Amputation is a special type of trauma. Mechanism of trauma-induced damage to the liver and the effects of hydrogen sulfide (H 2 S) on the liver remain unclear. <br> OBJECTIVE:To explore the mechanism of hepatic damage in rats of postoperative amputation, and how H 2 S exerts effects on liver function. <br> METHODS:Wistar rats and Sprague-Dawley rats were equal y and randomly divided into normal group, postoperative 6-, 12-, 24-and 72-hour groups, sodium hydrosulfide (NaHS) group, and propargyl glycine group, as wel as normal group, postoperative 6-hour group, HaHS group, and propargyl glycine group. Except the normal group, the structure 1.2-1.4 cm above the left knee was completely transected in rats of other groups. Blood vessels were ligated, and then left femoral vein and femoral artery were cut to establish rat models of amputation in the left hind limb. In the NaHS and propargyl glycine groups, 28 μmol/kg NaHS and 50 mg/kg propargyl glycine were intraperitoneal y injected immediately after amputation. <br> RESULTS AND CONCLUSION:Compared with the normal group, traumatic changes in rat liver cel s and mitochondrial structure were seen, and plasma and liver myeloperoxidase, malondialdehyde, H 2 S/cystathionineγ-lyase levels, liver mitochondrial respiratory control rate, membrane potential and ATP activity were significantly lower in the postoperative 6-hour groups (P<0.05). After NaHS intervention, H 2 S/cystathionineγ-lyase level and above indicators were significantly higher in the postoperative 6-hour groups (P<0.05), but plasma transaminase did not significantly alter (P>0.05). After treatment with propargyl glycine, above indicators except mitochondrial indexes were further decreased, and transaminase was significantly reduced (P<0.05). These findings suggest that H 2 S can reduce lipid peroxidation, inflammatory reaction, and make the mitochondrial function improved significantly, but did not reduce the damage of liver function in rat models after amputation.