中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
28期
5216-5222
,共7页
肖频%庞奕辉%彭朋%薄海
肖頻%龐奕輝%彭朋%薄海
초빈%방혁휘%팽붕%박해
组织构建%组织构建细胞学实验%肌肉肌腱韧带%慢性低氧%α-硫辛酸%线粒体%Sirtuin-3%氧化应激%骨骼肌%省级基金
組織構建%組織構建細胞學實驗%肌肉肌腱韌帶%慢性低氧%α-硫辛痠%線粒體%Sirtuin-3%氧化應激%骨骼肌%省級基金
조직구건%조직구건세포학실험%기육기건인대%만성저양%α-류신산%선립체%Sirtuin-3%양화응격%골격기%성급기금
tissue construction%cytology experiment in tissue construction%muscle tendon ligament%chronic hypoxia%α-lipoic acid%mitochondria%Sirtuin-3%oxidative stress%skeletal muscle%provincial grants-supported paper
背景:α-硫辛酸被誉为“全能抗氧化剂”和“线粒体营养剂”,但其是否可用于慢性低氧骨骼肌的防护,及其相关机制尚不清楚。目的:观察α-硫辛酸对慢性低氧大鼠骨骼肌线粒体活性氧生成及抗氧化酶系的作用,并探讨α-硫辛酸作用的相关信号通路。方法:将36只 SD 大鼠随机分为常氧对照组、单纯低氧组和单纯低氧+α-硫辛酸组。低氧干预为常压低氧帐篷,氧体积分数设定为11.3%;α-硫辛酸干预为标准饲料中添加α-硫辛酸(0.25%)。各种干预均持续4周。结果与结论:α-硫辛酸显著上调Sirtuin-3表达,提高线粒体ATP合成活力和膜电位,上调线粒体态3呼吸速率、呼吸控制比和磷氧比,下调态4呼吸速率,促进并上调锰超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶等线粒体抗氧化酶系活性,从而抑制线粒体H2O2产生速率,降低线粒体丙二醛含量。表明α-硫辛酸可提高慢性低氧骨骼肌线粒体能量代谢效率,抑制活性氧生成。并通过提高线粒体抗氧化酶系活性,抑制低氧诱导的氧化应激。α-硫辛酸对低氧骨骼肌线粒体的保护效应可能与其上调态3呼吸速率有关。
揹景:α-硫辛痠被譽為“全能抗氧化劑”和“線粒體營養劑”,但其是否可用于慢性低氧骨骼肌的防護,及其相關機製尚不清楚。目的:觀察α-硫辛痠對慢性低氧大鼠骨骼肌線粒體活性氧生成及抗氧化酶繫的作用,併探討α-硫辛痠作用的相關信號通路。方法:將36隻 SD 大鼠隨機分為常氧對照組、單純低氧組和單純低氧+α-硫辛痠組。低氧榦預為常壓低氧帳篷,氧體積分數設定為11.3%;α-硫辛痠榦預為標準飼料中添加α-硫辛痠(0.25%)。各種榦預均持續4週。結果與結論:α-硫辛痠顯著上調Sirtuin-3錶達,提高線粒體ATP閤成活力和膜電位,上調線粒體態3呼吸速率、呼吸控製比和燐氧比,下調態4呼吸速率,促進併上調錳超氧化物歧化酶、穀胱甘肽過氧化物酶、過氧化氫酶等線粒體抗氧化酶繫活性,從而抑製線粒體H2O2產生速率,降低線粒體丙二醛含量。錶明α-硫辛痠可提高慢性低氧骨骼肌線粒體能量代謝效率,抑製活性氧生成。併通過提高線粒體抗氧化酶繫活性,抑製低氧誘導的氧化應激。α-硫辛痠對低氧骨骼肌線粒體的保護效應可能與其上調態3呼吸速率有關。
배경:α-류신산피예위“전능항양화제”화“선립체영양제”,단기시부가용우만성저양골격기적방호,급기상관궤제상불청초。목적:관찰α-류신산대만성저양대서골격기선립체활성양생성급항양화매계적작용,병탐토α-류신산작용적상관신호통로。방법:장36지 SD 대서수궤분위상양대조조、단순저양조화단순저양+α-류신산조。저양간예위상압저양장봉,양체적분수설정위11.3%;α-류신산간예위표준사료중첨가α-류신산(0.25%)。각충간예균지속4주。결과여결론:α-류신산현저상조Sirtuin-3표체,제고선립체ATP합성활력화막전위,상조선립체태3호흡속솔、호흡공제비화린양비,하조태4호흡속솔,촉진병상조맹초양화물기화매、곡광감태과양화물매、과양화경매등선립체항양화매계활성,종이억제선립체H2O2산생속솔,강저선립체병이철함량。표명α-류신산가제고만성저양골격기선립체능량대사효솔,억제활성양생성。병통과제고선립체항양화매계활성,억제저양유도적양화응격。α-류신산대저양골격기선립체적보호효응가능여기상조태3호흡속솔유관。
BACKGROUND: α-lipoic acid is named as “nature antioxidant” and “mitochondrial nutrition”. But it is unclear whether α-lipoic acid can be used to protect skeletal muscle with chronic hypoxia exposure, as wel as the relative mechanism. OBJECTIVE: To observe the effect of α-lipoic acid on the antioxidant enzymes and oxidative stress in rat skeletal muscle with chronic hypoxia exposure, and to investigate the relative signaling pathway of α-lipoic acid. METHODS: Thirty-six Sprague Dawley rats were randomly divided into three groups: normoxia control group, hypoxia control group, and hypoxia+α-lipoic acid group. Rats in the hypoxia control group were subjected to hypoxia exposure in normobaric hypoxic tent with 11.3% oxygen concentration. Rats in the hypoxia+α-lipoic acid group were induced by adding α-lipoic acid (0.25%) in the normal diet. Al the interventions were lasted for 4 weeks. RESULTS AND CONCLUSION: α-lipoic acid in hypoxia could markedly enhance the mitochondrial Sirtuin-3 expression, improve the mitochondrial adenosine triphosphate synthesis activity and membrane potential, up-regulate the mitochondrial state 3 respiratory rate, respiratory control ratio and ratio of phosphorus to oxygen, down-regulate the mitochondrial state 4 respiratory rate and promote and up-regulate the activity of mitochondrial antioxidant enzymes such as manganese superoxide dismutase, glutathione peroxidase and catalase, thus inhibiting mitochondrial H2O2 generation rate and reducing mitochondrial malondialdehyde level. The results indicated that α-lipoic acid could improve the efficiency of energy metabolism of chronic hypoxia skeletal muscle mitochondria and inhibit reactive oxygen generation, and it could inhibit the oxidative stress through improving antioxidant enzyme activity of mitochondria. The protection mechanism of α-lipoic acid on hypoxia skeletal muscle mitochondria may be related to the increasing of mitochondrial state 3 respiratory rate.