首页> 中文期刊>中华老年医学杂志 >脂联素及其受体信号通路在肢体缺血预适应对心肌保护中的作用

脂联素及其受体信号通路在肢体缺血预适应对心肌保护中的作用

摘要

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.%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.

著录项

相似文献

  • 中文文献
  • 外文文献
  • 专利

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号