环球中医药
環毬中醫藥
배구중의약
GLOBAL TCM
2015年
7期
794-797
,共4页
刘鹏年%李忆兰%张路%谢飞%李剑瑜%武凡
劉鵬年%李憶蘭%張路%謝飛%李劍瑜%武凡
류붕년%리억란%장로%사비%리검유%무범
三七皂甙Rb1%慢性阻塞性肺疾病%线粒体
三七皂甙Rb1%慢性阻塞性肺疾病%線粒體
삼칠조대Rb1%만성조새성폐질병%선립체
Panax notoginseng saponins Rb1%Chronic obstructive pu1monary disease%Mito-chondria1
目的:探讨三七皂甙 Rb1对大鼠慢性阻塞性肺疾病( chronic obstructive pu1monary disease,COPD﹚线粒体的保护作用及作用机理。方法将40只大鼠随机分为4组,分别为对照组、COPD组、Rb110 mg/kg组和Rb120 mg/kg组。用烟熏法复制COPD大鼠模型,用低温差速离心法提取肺脏组织线粒体,紫外分光光度法测定肺脏线粒体呼吸链复合体Ⅰ、Ⅱ、Ⅲ、Ⅳ的活性及ATP合酶活性。用荧光分光光度计测量肺脏线粒体的膜电位,采用荧光标记与荧光偏振法测定线粒体膜偏振度,计算膜的微黏度。 ELⅠSA法检测肺脏线粒体分泌型磷脂酶A2(secretory phospho1ipase A2, sPLA2﹚的活性。结果 COPD组降低线粒体膜电位,增加膜的偏振度、微黏度,降低膜的津动性。Rb1组显著增加呼吸链复合体Ⅰ、Ⅲ、Ⅳ的活性( P<0.01﹚,提高ATP合酶活性( P<0.01﹚。生物物理学证实Rb1组增加线粒体膜电位,减低膜的偏振度、微黏度,增加膜的津动性。 Rb110 mg/kg和Rb120 mg/kg组均抑制sPLA2活性的升高(P<0.05,P<0.01﹚。结论三七皂甙Rb1通过保护大鼠肺脏线粒体结构与功能而起到防治COPD的作用。
目的:探討三七皂甙 Rb1對大鼠慢性阻塞性肺疾病( chronic obstructive pu1monary disease,COPD﹚線粒體的保護作用及作用機理。方法將40隻大鼠隨機分為4組,分彆為對照組、COPD組、Rb110 mg/kg組和Rb120 mg/kg組。用煙熏法複製COPD大鼠模型,用低溫差速離心法提取肺髒組織線粒體,紫外分光光度法測定肺髒線粒體呼吸鏈複閤體Ⅰ、Ⅱ、Ⅲ、Ⅳ的活性及ATP閤酶活性。用熒光分光光度計測量肺髒線粒體的膜電位,採用熒光標記與熒光偏振法測定線粒體膜偏振度,計算膜的微黏度。 ELⅠSA法檢測肺髒線粒體分泌型燐脂酶A2(secretory phospho1ipase A2, sPLA2﹚的活性。結果 COPD組降低線粒體膜電位,增加膜的偏振度、微黏度,降低膜的津動性。Rb1組顯著增加呼吸鏈複閤體Ⅰ、Ⅲ、Ⅳ的活性( P<0.01﹚,提高ATP閤酶活性( P<0.01﹚。生物物理學證實Rb1組增加線粒體膜電位,減低膜的偏振度、微黏度,增加膜的津動性。 Rb110 mg/kg和Rb120 mg/kg組均抑製sPLA2活性的升高(P<0.05,P<0.01﹚。結論三七皂甙Rb1通過保護大鼠肺髒線粒體結構與功能而起到防治COPD的作用。
목적:탐토삼칠조대 Rb1대대서만성조새성폐질병( chronic obstructive pu1monary disease,COPD﹚선립체적보호작용급작용궤리。방법장40지대서수궤분위4조,분별위대조조、COPD조、Rb110 mg/kg조화Rb120 mg/kg조。용연훈법복제COPD대서모형,용저온차속리심법제취폐장조직선립체,자외분광광도법측정폐장선립체호흡련복합체Ⅰ、Ⅱ、Ⅲ、Ⅳ적활성급ATP합매활성。용형광분광광도계측량폐장선립체적막전위,채용형광표기여형광편진법측정선립체막편진도,계산막적미점도。 ELⅠSA법검측폐장선립체분비형린지매A2(secretory phospho1ipase A2, sPLA2﹚적활성。결과 COPD조강저선립체막전위,증가막적편진도、미점도,강저막적진동성。Rb1조현저증가호흡련복합체Ⅰ、Ⅲ、Ⅳ적활성( P<0.01﹚,제고ATP합매활성( P<0.01﹚。생물물이학증실Rb1조증가선립체막전위,감저막적편진도、미점도,증가막적진동성。 Rb110 mg/kg화Rb120 mg/kg조균억제sPLA2활성적승고(P<0.05,P<0.01﹚。결론삼칠조대Rb1통과보호대서폐장선립체결구여공능이기도방치COPD적작용。
Objective To investigate the protection mechanism of panax notoginseng saponins Rb1 on mitochondria of rats with chronic obstructive pu1monary disease ( COPD﹚. Methods 40 rats were random1y divided into 4 groups: contro1 group, COPD group, 10 mg/kg Rb1 group and 20 mg/kg Rb1 group. COPD rat mode1s were estab1ished by using smoking method. Mitochondrias in rat 1ungs were extracted by using hypotherma1 differentia1 centrifugation method, and the activity of mitochondria1 respiratory comp1ex Ⅰ, Ⅱ, Ⅲ and Ⅳ in 1ungs was determined by using u1travio1et spectroscopy. Pu1monary mitochondria1 membrane potentia1 ( MMP﹚ was determined by using f1uorescence spectrophotometer. Po1arization degree of mitochondria1 membrane and microviscosity of membrane were determined and ca1cu1ate by using f1uorescence tagging and f1uorescence po1arization methods. The activity of secretory phospho1ipase A2 ( sPLA2﹚ secreted by pu1monary mitochondria was tested by using ELⅠSA. Results The mitochondria1 membrane potentia1 and membrane f1uidity were decreased, and po-1arization degree and microviscosity of mitochondria1 membrane were increased in rats in COPD group. The activity of mitochondria1 respiratory comp1exⅠ,Ⅲ andⅣ and ATP synthase were increased significant1y in rats in Rb1 group ( P<0. 01﹚. An increase in mitochondria1 membrane potentia1 and membrane f1uidity and a decrease in po1arization degree and microviscosity of mitochondria1 membrane in rats of Rb1 group was proved by biophysio1ogy. 10 mg/kg and 20 mg/kg Rb1cou1d inhibit the sPLA2 activity ( P<0. 05, P<0. 01﹚. Conclusion Panax notoginseng saponins Rb1 cou1d prevent and treat COPD through
<br> protective effect on pu1monary mitichondria1 structure and function of rats.