您的位置: 专家智库 > >

国家重点基础研究发展计划(201ICB503901)

作品数:1 被引量:22H指数:1
发文基金:国家重点基础研究发展计划更多>>
相关领域:生物学农业科学更多>>

文献类型

  • 1篇中文期刊文章

领域

  • 1篇生物学
  • 1篇农业科学

主题

  • 1篇MYOCAR...
  • 1篇EDEMA
  • 1篇INHIBI...
  • 1篇CARDIO...
  • 1篇TONGXI...
  • 1篇SWINE

传媒

  • 1篇Chines...

年份

  • 1篇2013
1 条 记 录,以下是 1-1
排序方式:
Protein kinase A-mediated cardioprotection of Tongxinluo relates to the inhibition of myocardial inflammation, apoptosis, and edema in reperfused swine hearts被引量:22
2013年
Background Our previous studies have demonstrated that Tongxinluo (TXL), a traditional Chinese medicine, can protect hearts against no-reflow and reperfusion injury in a protein kinase A (PKA)-dependent manner. The present study was to investigate whether the PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis. Methods In a 90-minute ischemia and 3-hour reperfusion model, minipigs were randomly assigned to sham, control, TXL (0.05 g/kg, gavaged one hour prior to ischemia), and TXL + H-89 (a PKA inhibitor, intravenously and continuously infused at 1.0 μg/kg per minute) groups. Myocardial no-reflow, necrosis, edema, and apoptosis were determined by pathological and histological studies. Myocardial activity of PKA and myeloperoxidase was measured by colorimetric method. The expression of PKA, phosphorylated cAMP response element-binding protein (p-CREB) (Ser133), tumor necrosis factor a (TNF-a), P-selectin, apoptotic proteins, and aquaporins was detected by Western blotting analysis. Results TXL decreased the no-reflow area by 37.4% and reduced the infarct size by 27.0% (P〈0.05). TXL pretreatment increased the PKA activity and the expression of Ser133 p-CREB in the reflow and no-reflow myocardium (P 〈0.05). TXL inhibited the ischemia-reperfusion-induced elevation of myeloperoxidase activities and the expression of TNF-a and P-selectin, reduced myocardial edema in the left ventricle and the reflow and no-reflow areas and the expression of aquaporin-4, -8, and -9, and decreased myocytes apoptosis by regulation of apoptotic protein expression in the reflow and no-reflow myocardium. However, addition of the PKA inhibitor H-89 counteracted these beneficial effects of TXL. Conclusion PKA-mediated cardioprotection of TXL against no-reflow and reperfusion injury relates to the inhibition of myocardial inflammation, edema, and apoptosis in the reflow and no-reflow myocardium.
LI Xiang-dongYANG Yue-jinCHENG Yu-tongDOU Ke-feiTIAN YiMENG Xian-min
关键词:CARDIOPROTECTION
共1页<1>
聚类工具0