چاپ صفحه |  صفحه نخست سامانه |  نویسندگان |  اطلاعات تفضیلی |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| نویسنده | نفر چندم مقاله |
|---|---|
| علیرضا گرجانی | اول |
| آیسا رضابخش | دوم |
| رضا رهبرقاضی | سوم |
| نسرین مالکی دیزجی | پنجم |
| عنوان | متن |
|---|---|
| کلمات کلیدی | Autophagy, Rapamycin, High glucose, 3-Methyladenine, Endothelial Cells |
| خلاصه مقاله | Background: Many vascular injuries induced by diabetes, such as inefficient or aberrant neoangiogenesis, are caused by increased gloucose blood level. Autophagy represents a homeostatic cellular mechanism for the turnover of unfolds proteins and damaged organelles through a lysosome-dependent degradation manner. To better address whether stimulation or inhibition of autophagy could blunt or exacerbate cytotoxic effect of high glucose condition, two well-known autophagy modulators, namely rapamycin and hydroxychloroquine, were used in combination with 30 mM glucose condition on endothelial cells over course of 72 hour. Materials and Methods: Cells viability were measured by MTT assay. We used Griess method and TBARS assay to monitor changes in the levels of nitric oxide and malondialdehyde followed by flow cytometric analysis of ROS using DCFDA. To investigate the role of rapamycin and hydroxychloroquin on migration and in vitro angiogenic properties, we used routine scratch test and tubulogenesis assay, respectively. The expression of autophagic modulators LC3, Becline-1 and P62 was measured by using western blotting. Results: Our data showed that rapamycin increased cell survival in high glucose condition and hydroxychloroquine diminished it. Of interest, rapamycin significantly decreased the total levels of oxidative stress markers in both sets of environments. In contrast to hydroxychloroquin the stimulatory effects on cell migration and tubulogenesis were observed in all groups after exposure to rapamycin. Furthermore, autophagy flux was induced by rapamycin which blocked in presence of 3-Methyladenine. Conclusion: Together, rapamycin could protect endothelial cells from damages caused by high glucose condition. This effect was mediated by autophagy-dependent manner. |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| 1.jpg | 1398/08/20 | 2016867 | دانلود |
| Pages from Final_Booklet.pdf | 1398/08/20 | 283780 | دانلود |
| Final_Booklet.pdf | 1398/08/20 | 6876350 | دانلود |
