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- W4253896169 abstract "Abstract BackgroundOxidized low-density lipoprotein (ox-LDL)-induced an endothelial cell dysfunction is a significant event in the progression of atherosclerosis[1]. Even myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. MethodsHUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and Myr on HUVECs. The expression of EndMT markers was determined by Western blot analysis and immunocytochemistry. In addition, the relationship of GAS5 and miR-29a-3p was evaluated by RNA Fluorescent in Situ Hybridization (FISH) and RNA immunoprecipitation (RIP) assay. ResultsMyr preconditioning prevented ox-LDL-induced apoptosis, inflammatory response, and EndMT. GAS5 was upregulated in response to ox-LDL while it was down-regulated by Myr preconditioning. GAS5 over-expression attenuates Myr protective effects against ox-LDL–mediated HUVEC injury. Besides, miR-29a-3p is a target of GAS5 and down-regulated miR-29a-3p could further resuced the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signaling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. ConclusionMyr possessed an anti-inflammatory and anti-EndMT function against ox-LDL-induced HUVEC injury by regulating the GAS5/miR-29a-3p, indicating that Myr may have an important therapeutic function for atherosclerosis." @default.
- W4253896169 created "2022-05-12" @default.
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- W4253896169 date "2020-12-29" @default.
- W4253896169 modified "2023-10-18" @default.
- W4253896169 title "Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inflammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p" @default.
- W4253896169 doi "https://doi.org/10.21203/rs.3.rs-134985/v1" @default.
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