Background Inhibition of aging of vascular endothelial cells （VECs） may delay aging and prolong life. The goal of this study was to prepare anti-CD31 monoclonal antibody conjugated PEG-modified liposomes containing ...Background Inhibition of aging of vascular endothelial cells （VECs） may delay aging and prolong life. The goal of this study was to prepare anti-CD31 monoclonal antibody conjugated PEG-modified liposomes containing the AU-rich region connecting factor 1 （AUF1） gene （CD31-PILs-AUF1） and to explore the effects of targeting CD31-PILs-AUF1 to aging VECs. Methods The mean particle sizes of various PEGylated immunoliposomes （PILs） were measured using a Zetasizer Nano ZS. Gel retardation assay was used to confirm whether PILs had encapsulated the AUF1 plasmid successfully. Fluorescence microscopy and flow cytometry were used to quantify binding of CD31-PILs-AUF1 to target cells. Flow cytometry was also used to analyze the cell cycles of aging bEnd3 cells treated with CD31-PILs-AUF1. We also developed an aging mouse model by treating mice with D-galactose. Enzyme-linked immunosorbent assay （ELISA） was used to evaluate the levels of interleuldn-6 （IL-6） and tumor necrosis factor-or （TNF-ct）. The malondialdehyde （MDA） and the superoxide dismutase （SOD） levels were detected by commercial kits. Hematoxylin-eosin （HE） staining was used to determine whether treatment with CD31-PILs-AUF 1 was toxic to the mice. Results CD31-PILs-AUF 1 specifically could targeted bEnd3 VECs and increased the percentage of cells in the S and G2/M phases of aging bEnd3 cells. ELISA showed that content of the IL-6 and TNF-ct decreased in CD31-PILs-AUF1 group. The level of SOD increased, whereas MDA decreased in the CD31-PILs-AUF1 group. Additionally, CD31-PILs-AUF 1 was not toxic to the mice. Conclusion CD31-PILs-AUF 1 targets VECs and may delay their senescence.展开更多
基金This work was supported by grants from the Guangxi Natural Science Foundation （No. 2015GXNSFAA139217 and 2016GXNSFAA380231）, a grant from The Scientific Research Fund of Guangxi Education Department （No. YB2014057） entitled ＂AU-rich region connecting factor 1 targeted vascular endothelial cells for anti-aging＂, a grant from the Youth Foundation in Guangxi Medical Univer- sity （No. GXMUYSF201328）, a grant from the Undergraduate Innovative plan in Guangxi （No. 201510598012）, and a grant from the Guangxi Education Department Grant entitled ＂Innovation Project of Guangxi Graduate Educa- tion＂.
文摘Background Inhibition of aging of vascular endothelial cells （VECs） may delay aging and prolong life. The goal of this study was to prepare anti-CD31 monoclonal antibody conjugated PEG-modified liposomes containing the AU-rich region connecting factor 1 （AUF1） gene （CD31-PILs-AUF1） and to explore the effects of targeting CD31-PILs-AUF1 to aging VECs. Methods The mean particle sizes of various PEGylated immunoliposomes （PILs） were measured using a Zetasizer Nano ZS. Gel retardation assay was used to confirm whether PILs had encapsulated the AUF1 plasmid successfully. Fluorescence microscopy and flow cytometry were used to quantify binding of CD31-PILs-AUF1 to target cells. Flow cytometry was also used to analyze the cell cycles of aging bEnd3 cells treated with CD31-PILs-AUF1. We also developed an aging mouse model by treating mice with D-galactose. Enzyme-linked immunosorbent assay （ELISA） was used to evaluate the levels of interleuldn-6 （IL-6） and tumor necrosis factor-or （TNF-ct）. The malondialdehyde （MDA） and the superoxide dismutase （SOD） levels were detected by commercial kits. Hematoxylin-eosin （HE） staining was used to determine whether treatment with CD31-PILs-AUF 1 was toxic to the mice. Results CD31-PILs-AUF 1 specifically could targeted bEnd3 VECs and increased the percentage of cells in the S and G2/M phases of aging bEnd3 cells. ELISA showed that content of the IL-6 and TNF-ct decreased in CD31-PILs-AUF1 group. The level of SOD increased, whereas MDA decreased in the CD31-PILs-AUF1 group. Additionally, CD31-PILs-AUF 1 was not toxic to the mice. Conclusion CD31-PILs-AUF 1 targets VECs and may delay their senescence.
