广州医学院学报
廣州醫學院學報
엄주의학원학보
ACADEMIC JOURNAL OF GUANGZHOU MEDICAL COLLEGE
2014年
3期
9-13
,共5页
吴智业%卢俊江%唐诗彦%王兰青%赵路宁%邓菊%董颀%陈敏生
吳智業%盧俊江%唐詩彥%王蘭青%趙路寧%鄧菊%董頎%陳敏生
오지업%로준강%당시언%왕란청%조로저%산국%동기%진민생
压力负荷%心脏收缩功能%白藜芦醇%钙调控蛋白
壓力負荷%心髒收縮功能%白藜蘆醇%鈣調控蛋白
압력부하%심장수축공능%백려호순%개조공단백
pressure-overload%cardiac systolic function%resveratrol%Ca2+ handling proteins
目的:建立压力负荷性心衰大鼠模型,观察白藜芦醇对心肌收缩功能的保护作用及对心肌钙调控蛋白表达的影响。方法:以腹主动脉缩窄法建立大鼠压力过负荷心肌肥大模型,术后4周给予白藜芦醇[4 mg/(kg??d)]治疗4周和6周,用 IE 33彩超仪无创测量左室室壁厚度以及射血功能相关指标;实时定量 PCR 法检测左心室组织匀浆中 CaMKⅡ、PLB、NCX1、SERCA2、RYR2的 mRNA 的表达。结果:术后4周,与假手术组相比,腹主动脉缩窄大鼠左室室壁厚度、射血分数(EF)及收缩系数(FS)明显增高(P<0.05)。术后8周和10周,即药物干预后4周和6周,与假手术组相比,单纯手术组 EF 及 FS 明显降低(P<0.05);白藜芦醇干预组 EF 和 FS 较单纯手术组明显升高(P<0.05),且与假手术组比无显著差别。另外,与假手术组比较,单纯手术组 CaMKⅡ、PLB、NCX1的 mRNA 表达均明显增高(P<0.05),而 SERCA2、RYR2的 mRNA 表达明显降低(P<0.05);经白藜芦醇干预4周和六周后,CaMKⅡ、PLB、NCX1的 mRNA 表达明显下调(P<0.05);SERCA2、RYR2的 mRNA 表达则明显回升(P<0.05)。结论:白藜芦醇可显著改善压力负荷所致的心脏收缩功能损害,阻止心脏向失代偿阶段演变,其作用可能与调控心肌细胞中多种钙调节蛋白表达有关。
目的:建立壓力負荷性心衰大鼠模型,觀察白藜蘆醇對心肌收縮功能的保護作用及對心肌鈣調控蛋白錶達的影響。方法:以腹主動脈縮窄法建立大鼠壓力過負荷心肌肥大模型,術後4週給予白藜蘆醇[4 mg/(kg??d)]治療4週和6週,用 IE 33綵超儀無創測量左室室壁厚度以及射血功能相關指標;實時定量 PCR 法檢測左心室組織勻漿中 CaMKⅡ、PLB、NCX1、SERCA2、RYR2的 mRNA 的錶達。結果:術後4週,與假手術組相比,腹主動脈縮窄大鼠左室室壁厚度、射血分數(EF)及收縮繫數(FS)明顯增高(P<0.05)。術後8週和10週,即藥物榦預後4週和6週,與假手術組相比,單純手術組 EF 及 FS 明顯降低(P<0.05);白藜蘆醇榦預組 EF 和 FS 較單純手術組明顯升高(P<0.05),且與假手術組比無顯著差彆。另外,與假手術組比較,單純手術組 CaMKⅡ、PLB、NCX1的 mRNA 錶達均明顯增高(P<0.05),而 SERCA2、RYR2的 mRNA 錶達明顯降低(P<0.05);經白藜蘆醇榦預4週和六週後,CaMKⅡ、PLB、NCX1的 mRNA 錶達明顯下調(P<0.05);SERCA2、RYR2的 mRNA 錶達則明顯迴升(P<0.05)。結論:白藜蘆醇可顯著改善壓力負荷所緻的心髒收縮功能損害,阻止心髒嚮失代償階段縯變,其作用可能與調控心肌細胞中多種鈣調節蛋白錶達有關。
목적:건립압력부하성심쇠대서모형,관찰백려호순대심기수축공능적보호작용급대심기개조공단백표체적영향。방법:이복주동맥축착법건립대서압력과부하심기비대모형,술후4주급여백려호순[4 mg/(kg??d)]치료4주화6주,용 IE 33채초의무창측량좌실실벽후도이급사혈공능상관지표;실시정량 PCR 법검측좌심실조직균장중 CaMKⅡ、PLB、NCX1、SERCA2、RYR2적 mRNA 적표체。결과:술후4주,여가수술조상비,복주동맥축착대서좌실실벽후도、사혈분수(EF)급수축계수(FS)명현증고(P<0.05)。술후8주화10주,즉약물간예후4주화6주,여가수술조상비,단순수술조 EF 급 FS 명현강저(P<0.05);백려호순간예조 EF 화 FS 교단순수술조명현승고(P<0.05),차여가수술조비무현저차별。령외,여가수술조비교,단순수술조 CaMKⅡ、PLB、NCX1적 mRNA 표체균명현증고(P<0.05),이 SERCA2、RYR2적 mRNA 표체명현강저(P<0.05);경백려호순간예4주화륙주후,CaMKⅡ、PLB、NCX1적 mRNA 표체명현하조(P<0.05);SERCA2、RYR2적 mRNA 표체칙명현회승(P<0.05)。결론:백려호순가현저개선압력부하소치적심장수축공능손해,조지심장향실대상계단연변,기작용가능여조공심기세포중다충개조절단백표체유관。
Objective: To observe the protection of resveratrol on cardiac contractile function and its regulation on the expression of Ca2+ hanlding proteins in rats with pressure overload. Methods Pressure-overload cardiac hypertrophy model was built by abdominal aortic constriction (AAC) in rats. 4 weeks after the operation, the rats were treated with resveratrol (4mg/ (kg??day) for 4 weeks and 6 weeks. IE 33 echocardiography was used to measure the thickness of walls and ejection functions of left ventricle(LV). The mRNA expression of Ca2+hanlding proteins including CaMK Ⅱ、PLB、NCX1、SERCA2、 RYR2 were detected with Real-time PCR assay. Results 4 weeks after the operation, the thickness of LV walls, ejection fraction (EF) and fractional shortening (FS) in AAC rats were significantly higher than those in sham group (P<0.05). 8 and 10 weeks after operation, namely 4 and 6 weeks after treatment with resveratrol, EF and FS in AAC group were significantly reduced compared with sham rats (P<0.05). However, EF and FS in rats treated with resveratrol were significantly higher than banded rats, and had no obvious difference compared with sham group (P<0.05). Moreover, compare to sham rats, the mRNA expressions of CaMKⅡ、PLB、NCX1 in AAC group were remarkably higher, accompanied with decreased SERCA2、RYR2(P<0.05). After 4 and 6-week treatment with resveratrol, the mRNA expressions of CaMKⅡ、PLB、NCX1 were down-regulated effectively, and SERCA2、RYR2 were distinctly elevated (P<0.05). Conclusion Resveratrol ameliorated cardiac systolic dysfunction caused by pressure overload, and prevented the transitions of cardiac function from compensatory to decompensatory stage, which might work through controlling and regulating the expression of various Ca2+ handling proteins in myocardial cells.