التفاصيل البيبلوغرافية
| العنوان: |
Pitavastatin up-regulates eNOS production by suppressing miR-155 expression in lipopolysaccharide-stimulated human umbilical vein endothelial cells. |
| المؤلفون: |
Jing, Changqin1,2, Guo, Menglong1,2, Bao, Xiaodan1,2, Li, Tianhan1,2, Lin, Juntang1,2, Lu, Xinjie1,2, Wang, Wenfeng1,2 wwf200594@163.com |
| المصدر: |
Cardiovascular Therapeutics. Oct2017, Vol. 35 Issue 5, pn/a-N.PAG. 6p. |
| مصطلحات موضوعية: |
*LIPOPOLYSACCHARIDES, *UMBILICAL veins, *ENDOTHELIAL cells, *ATHEROSCLEROSIS, *MESSENGER RNA |
| مستخلص: |
Aim Pitavastatin (Pit) has been proved to efficiently inhibit the onset and progression of atherosclerosis. However, the mechanism by which Pit exerts nonlipid-related effects, such as antiinflammatory actions, is not quite clear. Our study aimed at investigating the effect of Pit on the expression of endothelial NO synthase ( eNOS) and miR-155 in LPS-stimulated HUVECs to reveal the antiinflammatory mechanism of pitavastatin. Methods HUVECs were isolated from newborn umbilical cords and used in the experiments at passages 2-5. Cells were treated with LPS (0.05, 0.1, 1 μg/L) or LPS (0.1 μg/L)+Pit (0.01, 0.1, 1 μmol/L), untreated cells were used as control. For LPS+Pit induction, cells were firstly incubated with Pit for 1 hour before coincubation with LPS for 24 hours. eNOS mRNA and miR-155 were detected by RT- PCR, and Western blotting was used to detect protein expression of eNOS. Results Treatment of HUVECs with LPS enhanced the expression of miR-155 and reduced the expression of eNOS in mRNA and protein level in a dose-dependent manner as revealed by RT- PCR and Western blotting, respectively. Pitavastatin ameliorated LPS-induced endothelial dysfunction through upregulation of eNOS expression and downregulation of miR-155 expression. Conclusion Pitavastatin increases eNOS expression and inhibits of LPS-induced miR-155 expression. [ABSTRACT FROM AUTHOR] |
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