湖北科技学院学报(医学版)
湖北科技學院學報(醫學版)
호북과기학원학보(의학판)
JOURNAL OF XIANNING UNIVERSITY (MEDICAL SCIENCES)
2013年
4期
277-280
,共4页
余良主%韩璐%孟巍%王柏军%王帮华
餘良主%韓璐%孟巍%王柏軍%王幫華
여량주%한로%맹외%왕백군%왕방화
人参皂苷Rg1%血管紧张素Ⅱ%心肌细胞%TNF-α%IL-1β
人參皂苷Rg1%血管緊張素Ⅱ%心肌細胞%TNF-α%IL-1β
인삼조감Rg1%혈관긴장소Ⅱ%심기세포%TNF-α%IL-1β
Ginsenoside Rg1%AngiotensinⅡ%Cardiomyocyte%Tumor necrosis factor-α%Interleukin-1β
目的探讨传统中药人参皂苷Rg1对血管紧张素Ⅱ( AngⅡ)所诱发心肌肥大的影响。方法采用酶消化法分离新生大鼠心室肌细胞,培养心肌细胞随机分为3组:正常对照组、Ang Ⅱ组、AngⅡ+Rg1组。在接受药物处理24h后,检测心肌细胞总蛋白含量,β-MHC、TNF-α和IL-1β的mRNA表达量。结果 Ang Ⅱ处理导致培养心肌细胞的总蛋白含量以及β-MHC mRNA表达量显著增加,提示心肌肥大的发生;人参皂苷Rg1显著抑制了Ang Ⅱ的促心肌细胞肥大作用。同时,AngⅡ增加心肌细胞对TNF-α和IL -1βmRNA表达的效应也被人参皂苷Rg1所抑制。结论人参皂苷Rg1抑制了 AngⅡ诱导的心肌细胞肥大以及心肌细胞对炎性介质TNF-α、IL-1β的释放,这可能是人参皂苷Rg1对心脏疾病具有保护作用的细胞学基础。
目的探討傳統中藥人參皂苷Rg1對血管緊張素Ⅱ( AngⅡ)所誘髮心肌肥大的影響。方法採用酶消化法分離新生大鼠心室肌細胞,培養心肌細胞隨機分為3組:正常對照組、Ang Ⅱ組、AngⅡ+Rg1組。在接受藥物處理24h後,檢測心肌細胞總蛋白含量,β-MHC、TNF-α和IL-1β的mRNA錶達量。結果 Ang Ⅱ處理導緻培養心肌細胞的總蛋白含量以及β-MHC mRNA錶達量顯著增加,提示心肌肥大的髮生;人參皂苷Rg1顯著抑製瞭Ang Ⅱ的促心肌細胞肥大作用。同時,AngⅡ增加心肌細胞對TNF-α和IL -1βmRNA錶達的效應也被人參皂苷Rg1所抑製。結論人參皂苷Rg1抑製瞭 AngⅡ誘導的心肌細胞肥大以及心肌細胞對炎性介質TNF-α、IL-1β的釋放,這可能是人參皂苷Rg1對心髒疾病具有保護作用的細胞學基礎。
목적탐토전통중약인삼조감Rg1대혈관긴장소Ⅱ( AngⅡ)소유발심기비대적영향。방법채용매소화법분리신생대서심실기세포,배양심기세포수궤분위3조:정상대조조、Ang Ⅱ조、AngⅡ+Rg1조。재접수약물처리24h후,검측심기세포총단백함량,β-MHC、TNF-α화IL-1β적mRNA표체량。결과 Ang Ⅱ처리도치배양심기세포적총단백함량이급β-MHC mRNA표체량현저증가,제시심기비대적발생;인삼조감Rg1현저억제료Ang Ⅱ적촉심기세포비대작용。동시,AngⅡ증가심기세포대TNF-α화IL -1βmRNA표체적효응야피인삼조감Rg1소억제。결론인삼조감Rg1억제료 AngⅡ유도적심기세포비대이급심기세포대염성개질TNF-α、IL-1β적석방,저가능시인삼조감Rg1대심장질병구유보호작용적세포학기출。
Objective To determine the effect of ginsenoside Rg 1 on angiotensinⅡ ( AngⅡ)-induced myocardial hypertrophy .Methods Cardiomyocytes were isolated from 1~3 days old Sprague-Dawley rats and then randomly divided into 3 groups:normal control,Ang Ⅱgroup,Ang Ⅱ+Rg1 group.After 24h treatment, cardiomyocytes were collected to determine the total protein content by Lowry’ s method, and β-myosin heavy chain (β-MHC) ,TNF-α,and IL-1βmRNA expression was detected by Real-time PCR.Results Ang Ⅱ in-duced cardiomyocyte hypertrophy as evidenced by increased total protein content and enhanced expression of β-MHC mRNA.Ginsenoside Rg1 significantly inhibited these hypertrophic responses , suppressed AngⅡ-in-duced increase of TNF-αand IL-1βmRNA expression in cardiomyocytes .Conclusion Ginsenoside Rg1 can in-hibite cardiomyocyte hypertrophy induced by AngⅡ-and increase the release of inflammatory mediators such as TNF-αand IL-1β,which may be the cellular basis for its protective role in cardiac diseases .