scholarly journals Notoginsenoside R1 Protects HUVEC Against Oxidized Low Density Lipoprotein (Ox-LDL)-Induced Atherogenic Response via Down-Regulating miR-132

2018 ◽  
Vol 51 (4) ◽  
pp. 1739-1750 ◽  
Author(s):  
Changgeng Fu ◽  
Dexin Yin ◽  
Haiying Nie ◽  
Dajun Sun
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Matrix Gla Protein ◽  
Cell Counting ◽  
Intercellular Adhesion Molecule ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Qrt Pcr ◽  
Induced Apoptosis

Background/Aims: Radix notoginseng is a well-known traditional Chinese herbal medicine, has extensively pharmacological activities in cardiovascular system. Notoginsenoside R1 (NGR1) is one main active ingredient of Radix notoginseng. The purpose of this study was to evaluate the functional effects of NGR1 on atherosclerosis (AS). Methods: Human umbilical vascular endothelial cells (HUVECs) were subjected to oxidized low density lipoprotein (ox-LDL), before which cells were preconditioned with NGR1. Cell Counting Kit-8 (CCK-8) assay, flow cytometry, Transwell assay, quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were carried out to assess the impacts of ox-LDL and NGR1 on HUVECs. Besides, the expression of microRNA-132 (miR-132), and the regulatory role of miR-132 in Matrix Gla Protein (MGP) expression were measured by qRT-PCR and Western blot. Results: NGR1 pre-conditioning prevented ox-LDL-induced apoptosis, migration and overproduction of Monocyte Chemoattractant Protein 1 (MCP-1) and Intercellular Adhesion Molecule 1 (ICAM-1). miR-132 was up-regulated in response to ox-LDL while was down-regulated by NGR1 pre-conditioning. The protective actions of NGR1 in ox-LDL-treated HUVECs were enhanced by miR-132 inhibitor, while were attenuated by miR-132 mimic. Besides, the up-regulated miR-132 could further decrease the expression of MGP, which acted as an anti-migratory and anti-adhesive factor. Furthermore, ox-LDL-induced the activation of c-Jun N-terminal Kinase (JNK) and Nuclear Factor Kappa B (NF-κB) pathways were partially attenuated by NGR1, and were fully eliminated by NGR1 treatment together with MGP overexpression. Conclusion: NGR1 prevents ox-LDL-induced apoptosis, migration and adhesion-related molecule release in HUVECs possibly via down-regulating miR-132, and subsequent up-regulating MGP.

miR-155 inhibits oxidized low-density lipoprotein-induced apoptosis of RAW264.7 cells

2013 ◽  
Vol 382 (1-2) ◽  
pp. 253-261 ◽  
Author(s):  
Guo-fu Zhu ◽  
Li-xia Yang ◽  
Rui-wei Guo ◽  
Hong Liu ◽  
Yan-kun Shi ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Raw264.7 Cells ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Induced Apoptosis

scholarly journals Mitochondria hyperpolarization is an early event in oxidized low-density lipoprotein-induced apoptosis in Caco-2 intestinal cells

FEBS Letters ◽  
2002 ◽  
Vol 523 (1-3) ◽  
pp. 200-206 ◽  
Author(s):  
Claudio Giovannini ◽  
Paola Matarrese ◽  
Beatrice Scazzocchio ◽  
Massimo Sanchez ◽  
Roberta Masella ◽  
...  
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Intestinal Cells ◽  
Early Event ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Induced Apoptosis

scholarly journals Myricetin Ameliorates Ox-LDL-induced HUVECs Apoptosis and Inflammation via lncRNA GAS5 Upregulating the Expression of miR-29a-3p

2020 ◽  
Author(s):  
Yunpeng Bai ◽  
Qingliang Chen ◽  
Nan Jiang ◽  
zhigang guo
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

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.

scholarly journals Myricetin ameliorates ox-LDL-induced HUVECs apoptosis and inflammation via lncRNA GAS5 upregulating the expression of miR-29a-3p

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yunpeng Bai ◽  
Xiankun Liu ◽  
Qingliang Chen ◽  
Tongyun Chen ◽  
Nan Jiang ◽  
...  
Keyword(s):  
Western Blot ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Cell Counting ◽  
Protective Effects ◽  
Cell Dysfunction ◽  
Rna Immunoprecipitation ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation ◽  
Relationship Of

AbstractOxidized low-density lipoprotein (ox-LDL)-induced endothelial cell dysfunction is a significant event in the progression of atherosclerosis. Even Myricetin (Myr) has been exhibited strong antioxidant potency, the effect on atherosclerosis is still elusive. HUVECs were subjected to ox-LDL, before which cells were preconditioned with Myr. Cell Counting Kit-8 assay, flow cytometry, quantitative real-time polymerase chain reaction 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 and RNA immunoprecipitation assay. Myr 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 reduce the effects of GAS5 in ox-LDL–mediated HUVEC. Furthermore, Myr inactivated the TLR4/NF-κB signalling pathway in ox-LDL-treated HUVEC by down-regulating GAS5 or upregulating miR-26a-5p. Myr 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.

scholarly journals Effects of Equol on Oxidized Low-Density Lipoprotein-Induced Apoptosis in Endothelial Cells

2009 ◽  
Vol 16 (3) ◽  
pp. 239-249 ◽  
Author(s):  
Masumi Kamiyama ◽  
Yoshimi Kishimoto ◽  
Mariko Tani ◽  
Kazunori Utsunomiya ◽  
Kazuo Kondo
Keyword(s):  
Endothelial Cells ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Oxidized Low Density Lipoprotein ◽  
Induced Apoptosis
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