Abstract:
OBJECTIVE:The goals of this study were to observe how luteolin protects endothelial cells (ECs) from injury stimulated by Angiotensin II (Ang II), investigate the role of vascular endothelial dysfunction in vascular smooth muscle cell proliferation and migration in vitro and investigate its primary mechanism of action. METHODS:A non-contact coculture system was established using a transwell system; ECs were cultured in the lower wells, while the smooth muscle cells (SMCs) were cultured in the upper wells. Cell proliferation was assessed by the MTT assay. The number of SMCs that migrated through the membrane of transwell system were observed and counted. The expression levels of various proteins (VEGF, p-Akt, Nox4) expressed in ECs were determined by Western blotting. VEGF mRNA expression was detected by reverse transcription-polymerase chain reaction (RT-PCR). The supernatants of ECs were measured by enzyme linked immunosorbent assay (ELISA) to assay VEGF concentration. RESULTS:Ang II-stimulated ECs significantly increased the proliferation and migration of SMCs, and these effects were inhibited by luteolin pretreatment. Luteolin suppressed the Ang II-induced upregulation of Nox4, p-AKT and VEGF expression in ECs. CONCLUSION:These results demonstrate that luteolin is capable of inhibiting endothelial dysfunction induced by Ang II by suppressing the upregulation of Nox4, p-Akt and VEGF, thereby restraining the proliferation and migration of SMCs induced by injured ECs.
journal_name
Curr Pharm Biotechnoljournal_title
Current pharmaceutical biotechnologyauthors
Ding H,Li D,Zhang Y,Zhang T,Zhu H,Xu T,Luo Y,Wang Cdoi
10.2174/1389201015666140113113843subject
Has Abstractpub_date
2014-01-01 00:00:00pages
1009-15issue
12eissn
1389-2010issn
1873-4316pii
CPB-EPUB-58599journal_volume
14pub_type
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journal_title:Current pharmaceutical biotechnology
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journal_title:Current pharmaceutical biotechnology
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abstract:: ...
journal_title:Current pharmaceutical biotechnology
pub_type: 社论
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