中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2012年
5期
434-437
,共4页
心肌%再灌注损伤%受体,脂联素%信号传导%1磷脂酰肌醇-3激酶
心肌%再灌註損傷%受體,脂聯素%信號傳導%1燐脂酰肌醇-3激酶
심기%재관주손상%수체,지련소%신호전도%1린지선기순-3격매
Myocardium%Reperfusion injury%Receptors,adiponectin%Signal transduction%1-phosphatidylinositol 3-kinase
目的 探讨心肌脂联素(ADP)及其受体(ADPR1)的磷脂酰肌醇-3激酶(PI3k)/磷酸化的蛋白激酶B(p-Akt)通路是否介导了肢体缺血预适应对心肌的保护作用. 方法 30只健康雄性SD大鼠,随机分为假手术组、心肌缺血-再灌注损伤组(MIRI组)、肢体缺血预适应(LIPC)组、PI3k特异性抑制剂(LY294002)预处理组和LIPC+ LY294002预处理组.分别采用RT-PCR法和Western blot法检测心肌组织中ADP和ADPR1的mRNA及PI3k和p-Akt蛋白的表达水平. 结果 与假手术组相比,MIRI组ADP (0.53±0.07比0.74±0.08)和ADPR1 (0.52±0.02比0.72±0.04)的mRNA值明显减少(P＜0.05)；与MIRI组相比,LIPC组上调ADP(0.72±0.21)和ADPR1(0.80±0.02)的mRNA值(P＜0.05),LY294002则下调ADP (0.49±0.07)和ADPR1(0.52±0.02)的mRNA值(P＜0.05); LY294002+ LIPC组ADP和ADPR1的mRNA值,与MIRI组比较差异无统计学意义(P＞0.05).与假手术组相比,MIRI组PI3k(3.85±0.23)和p-Akt( 3.77±0.32)蛋白水平表达降低(P＜0.05),LIPC组PI3k(2.65±0.32)和p-Akt(2.26±0.27)蛋白水平较MIRI组表达增加(P＜0.05),LY294002组的PI3k和p-Akt蛋白几乎不表达(P＜0.05); LIPC+LY294002组大鼠心肌组织PI3k和p-Akt蛋白表达与LY90024预处理组相比差异无统计学意义(P＞0.05).心肌ADP水平与ADPR1 mRNA、PI3K和P-Akt蛋白水平呈正相关(r=0.886、0.756、0.745,P＜0.05). 结论 肢体缺血预适应通过激活ADP/PI3k/Akt信号通路发挥对心肌再灌注损伤的保护性作用.
目的 探討心肌脂聯素(ADP)及其受體(ADPR1)的燐脂酰肌醇-3激酶(PI3k)/燐痠化的蛋白激酶B(p-Akt)通路是否介導瞭肢體缺血預適應對心肌的保護作用. 方法 30隻健康雄性SD大鼠,隨機分為假手術組、心肌缺血-再灌註損傷組(MIRI組)、肢體缺血預適應(LIPC)組、PI3k特異性抑製劑(LY294002)預處理組和LIPC+ LY294002預處理組.分彆採用RT-PCR法和Western blot法檢測心肌組織中ADP和ADPR1的mRNA及PI3k和p-Akt蛋白的錶達水平. 結果 與假手術組相比,MIRI組ADP (0.53±0.07比0.74±0.08)和ADPR1 (0.52±0.02比0.72±0.04)的mRNA值明顯減少(P＜0.05)；與MIRI組相比,LIPC組上調ADP(0.72±0.21)和ADPR1(0.80±0.02)的mRNA值(P＜0.05),LY294002則下調ADP (0.49±0.07)和ADPR1(0.52±0.02)的mRNA值(P＜0.05); LY294002+ LIPC組ADP和ADPR1的mRNA值,與MIRI組比較差異無統計學意義(P＞0.05).與假手術組相比,MIRI組PI3k(3.85±0.23)和p-Akt( 3.77±0.32)蛋白水平錶達降低(P＜0.05),LIPC組PI3k(2.65±0.32)和p-Akt(2.26±0.27)蛋白水平較MIRI組錶達增加(P＜0.05),LY294002組的PI3k和p-Akt蛋白幾乎不錶達(P＜0.05); LIPC+LY294002組大鼠心肌組織PI3k和p-Akt蛋白錶達與LY90024預處理組相比差異無統計學意義(P＞0.05).心肌ADP水平與ADPR1 mRNA、PI3K和P-Akt蛋白水平呈正相關(r=0.886、0.756、0.745,P＜0.05). 結論 肢體缺血預適應通過激活ADP/PI3k/Akt信號通路髮揮對心肌再灌註損傷的保護性作用.
목적 탐토심기지련소(ADP)급기수체(ADPR1)적린지선기순-3격매(PI3k)/린산화적단백격매B(p-Akt)통로시부개도료지체결혈예괄응대심기적보호작용. 방법 30지건강웅성SD대서,수궤분위가수술조、심기결혈-재관주손상조(MIRI조)、지체결혈예괄응(LIPC)조、PI3k특이성억제제(LY294002)예처리조화LIPC+ LY294002예처리조.분별채용RT-PCR법화Western blot법검측심기조직중ADP화ADPR1적mRNA급PI3k화p-Akt단백적표체수평. 결과 여가수술조상비,MIRI조ADP (0.53±0.07비0.74±0.08)화ADPR1 (0.52±0.02비0.72±0.04)적mRNA치명현감소(P＜0.05)；여MIRI조상비,LIPC조상조ADP(0.72±0.21)화ADPR1(0.80±0.02)적mRNA치(P＜0.05),LY294002칙하조ADP (0.49±0.07)화ADPR1(0.52±0.02)적mRNA치(P＜0.05); LY294002+ LIPC조ADP화ADPR1적mRNA치,여MIRI조비교차이무통계학의의(P＞0.05).여가수술조상비,MIRI조PI3k(3.85±0.23)화p-Akt( 3.77±0.32)단백수평표체강저(P＜0.05),LIPC조PI3k(2.65±0.32)화p-Akt(2.26±0.27)단백수평교MIRI조표체증가(P＜0.05),LY294002조적PI3k화p-Akt단백궤호불표체(P＜0.05); LIPC+LY294002조대서심기조직PI3k화p-Akt단백표체여LY90024예처리조상비차이무통계학의의(P＞0.05).심기ADP수평여ADPR1 mRNA、PI3K화P-Akt단백수평정정상관(r=0.886、0.756、0.745,P＜0.05). 결론 지체결혈예괄응통과격활ADP/PI3k/Akt신호통로발휘대심기재관주손상적보호성작용.
Objective To investigate the myocardial protection of adiponectin (ADP) /adiponectin receptor 1 (ADPR1) related-signal pathway in rats with limb ischemic preconditioning.Methods Thirty SD male rats were randomly divided into sham-operation group,myocardial ischemia reperfusion injury (MIRI) group,limb ischemic preconditioning (LIPC) group,LY294002 (the PI3-specific inhibitor) pretreatment group and LY294002+LIPC group (n=10 each).The mRNA level of myocardial ADP and ADPR1,the protein expressions of phosphatidylinositol 3-kinase (PI3k)phosphorylated Akt (p-Akt) were determined by RT-PCR and Western blot,respectively. Results As compared with sham-operation group,the mRNA levels of ADP and ADPR1 in MIRI group were significantly decreased (0.53 ± 0.07 vs.0.74 ± 0.08 and 0.52 ± 0.02 vs.0.72 ± 0.04,P＜0.05).Compared with MIRI group,the mRNA levels of ADP (0.72±0.21) and ADPRI (0.80±0.023) in LIPC group were increased,ADP(0.49±0.07) and ADPR1 (0.52± 0.02) mRNA were decreased in LY294002 group (both P＜0.05),but there were no difference in ADP(0.70±0.16) and ADPR1(0.78±0.05) mRNA between LY294002+LIPC group and MIRI group.The protein levels of Pl3k and p-Akt were lower in MIRI group than in sham-operation group (3.85±0.23 vs.2.83±0.22and 3.77±0.32 vs.2.66±0.29,P＜0.05).In contrast to MIRI group,the yield of PI3k (2.65±0.32)and p-Akt(2.26±0.27) protein (P＜0.05) were increased in LIPC group,but there were unproductive protein of PI3k (3.75 ± 0.65) and p-Akt (4.01 ± 0.71) in LY294002 group with no differences versus the levels of PI3k (3.23 ± 0.48) and p-Akt (3.17 ± 0.54) in LY294002 + LIPC group. Conclusions Limb ischemic preconditioning may protect myocardium by promoting serum adiponectin levels,improving myocardial mRNA expressions of ADP and ADPR1,activating the ADP/PI3k/Akt signaling pathway in reperfusion injury.
