作者: Tiebing Zhu , Qi Yao , Wei Wang , Honghong Yao , Jie Chao
DOI: 10.1159/000443098
关键词:
摘要: Background/Aims: Inducible nitric oxide synthase (iNOS) plays a crucial role in ischemia/ reperfusion (I/R). Autophagy is involved irreversible cell injury and death under extreme conditions. However, whether iNOS mediates myocardial ischemia/reperfusion (I/R) endothelial cells via autophagy remains ill-defined. In this study, we examined I/Rmediated up-regulation of critical the modulation migration apoptosis human umbilical vein (HUVECs). Methods: expression was detected HUVECs using Western blotting analyses immunocytochemistry. An vitro scratch assay performed to detect migration. The markers ATG5, LC3B BECN were analysis adenovirus-mRFP-GFPLC3. pharmacological inhibitor 3-MA also applied confirm I/R. Results: I/R induced iNOS, which subsequently increased associated with autophagy. specific L-NAME abolished I/R-induced autophagy, while both attenuated by Conclusion: These findings suggested that regulates indicates new therapeutic strategy for individuals injury.