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oxidized low-density lipoprotein stimulates CD206 positive macrophages upregulating CD44 and CD133 expression in colorectal cancer with high-fat diet

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World Journal of Gastroenterology 2022年第34期28卷 4993-5006页

作者： Shi-Min Zheng Hao Chen Wei-Hong Sha Xiao-Fen Chen Jian-Bin Yin Xiao-Bo Zhu Zhong-Wen Zheng Juan Ma Department of Gastroenterology and Hepatology Guangdong Provincial People’s HospitalGuangdong Academy of Medical SciencesGuangzhou 510080Guangdong ProvinceChina Medical College Shantou UniversityShantou 515041Guangdong ProvinceChina Medical College Southern Medical UniversityGuangzhou 510515Guangdong ProvinceChina Center for Orthopaedic Surgery The Third Affiliated Hospital of Southern Medical UniversityGuangzhou 510630Guangdong ProvinceChina

BACKGROUND oxidized low-density lipoprotein(ox-LDL),which is abnormally increased in the serum of colorectal cancer(CRC)patients consuming a high-fat diet(HFD),may be one of the risk factors for the development of CRC.Ox-LDL exerts a regulatory effect on macrophages and may influence CRC through the tumor microenvironment.The role of ox-LDL in CRC remains unclear.AIM To investigate the role of ox-LDL through macrophages in HFD associated CRC.METHODS The expression of ox-LDL and CD206 was detected in colorectal tissues of CRC patients with hyperlipidemia and HFD-fed mice by immunofluorescence.We stimulated the macrophages with 20μg/mL ox-LDL and assessed the expression levels of CD206 and the cytokines by cell fluorescence and quantitative polymerase chain reaction.We further knocked down LOX-1,the surface receptor of ox-LDL,to confirm the function of ox-LDL in macrophages.Then,LoVo cells were co-cultured with the stimulated macrophages to analyze the CD44 and CD133 expression by western blot.RESULTS The expression of ox-LDL and the CD206 was significantly increased in the stroma of colorectal tissues of CRC patients with hyperlipidemia,and also upregulated in the HFD-fed mice.Moreover,an increased level of CD206 and decreased level of inducible nitric oxide synthase were observed in macrophages after ox-LDL continuous stimulation.Such effects were inhibited when the surface receptor LOX-1 was knocked down in macrophages.Ox-LDL could induce CD206+macrophages,which resulted in high expression of CD44 and CD133 in co-cultured LoVo cells.CONCLUSION Ox-LDL stimulates CD206+macrophages to upregulate CD44 and CD133 expression in HFD related CRC.

关键词： oxidized low-density lipoprotein CD206 positive macrophages CD44 CD133

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Inhibitory Effects of Simvastatin on oxidized low-density lipoprotein-lnduced Endoplasmic Reticulum Stress and Apoptosis in Vascular Endothelial Cells

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Chinese Medical Journal 2018年第8期131卷 950-955页

作者： Guo-Qiang Zhang Yong-Kang Tao Yong-Ping Bai Sheng-Tao Yan Shui-Ping Zhao Department of Emergency China-Japan Friendship Hospital Beijing 100029 China Department of Geriatric Medicine Xiangya Hospital Central South University Changsha Hunan 410008 China Department of Cardiology The Second Xiangya Hospital Central South University Changsha Hunan 410011 China

Background：oxidized low-density lipoprotein （ox-LDL）-induced oxidative stress and endothelial apoptosis are essential for atherosclerosis. Our previous study has shown that ox-LDL-induced apoptosis is mediated by the protein kinase RNA-like endoplasmic reticulum kinase （PERK）/eukaryotic translation initiation factor 2α-subunit （eIF2α）/CCAAT/enhancer-binding protein homologous protein （CHOP） endoplasmic reticulum （ER） stress pathway in endothelial cells. Statins are cholesterol-lowering drugs that exert pleiotropic effects including suppression of oxidative stress. This study aimed to explore the roles of simvastatin on ox-LDL-induced ER stress and apoptosis in endothelial cells.Methods：Human umbilical vein endothelial cells （HUVECs） were treated with simvastatin （0.1, 0.5, or 2.5 μmol/L） or DEVD-CHO （selective inhibitor of caspase-3, 100 μmol/L） for 1 h before the addition of ox-LDL （100 μg/ml） and then incubated for 24 h, and untreated cells were used as a control group. Apoptosis, expression of PERK, phosphorylation of eIF2α, CHOP mRNA level, and caspase-3 activity were measured. Comparisons among multiple groups were performed with one-way analysis of variance （ANOVA） followed by post hoc pairwise comparisons using Tukey’s tests. A value of P 〈 0.05 was considered statistically significant.Results：Exposure of HUVECs to ox-LDL resulted in a significant increase in apoptosis （31.9% vs. 4.9%, P 〈 0.05）. Simvastatin （0.1, 0.5, and 2.5 μmol/L） led to a suppression of ox-LDL-induced apoptosis （28.0%, 24.7%, and 13.8%, F = 15.039, all P 〈 0.05, compared with control group）. Ox-LDL significantly increased the expression of PERK （499.5%, P 〈 0.05） and phosphorylation of eIF2α （451.6%, P 〈 0.05）, if both of which in the control groups were considered as 100%. Simvastatin treatment （0.1, 0.5, and 2.5 μmol/L） blunted ox-LDL-induced expression of PERK （407.8%, 339.1%, and 187.5%, F = 10.121, all P 〈 0.05, compared with control group） and phosphorylation of eIF2α （407.8%, 339.1%, 187.5%, F = 11.430, all P 〈 0.05, compared w

关键词： Apoptosis Endoplasmic Reticulum Stress Endothelial Cells oxidized low-density lipoprotein Simvastatin

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Role of PERK/eIF2α/CHOP Endoplasmic Reticulum Stress Pathway in oxidized low-density lipoprotein Mediated Induction of Endothelial Apoptosis

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Biomedical and Environmental Sciences 2016年第12期29卷 868-876页

作者： TAO Yong Kang YU Pu Lin BAI Yong Ping YAN Sheng Tao ZHAO Shui Ping ZHANG Guo Qiang Departments of Emergency China-Japan Friendship HospitalBeijing 100029China Beijing Institution of Geriatrics Beijing HospitalBeijing 100730China Department of Geriatric Medicine Xiangya HospitalCentral South UniversityChangsha 410008HunanChina Department of Cardiology The Second Xiangya HospitalCentral South UniversityChangsha 410011HunanChina

Objective PERK/elF2/CHOP is a major signaling pathway mediating endoplasmic reticulum （ER） stress related with atherosclerosis. oxidized LDL （ox-LDL） also induces endothelial apoptosis and plays a vital role in the initiation and progression of atherosclerosis. The present study was conducted to explore the regulatory effect of ox-LDL on PERK/elF2a/CHOP signaling pathway in vascular endothelial cells. Methods The effects of ox-LDL on PERK and p-elF2a protein expression of primary human umbilical vein endothelial cells （HUVECs） were investigated by Western blot analysis. PERK gene silencing and selective elF2a phosphatase inhibitor, salubrinal were used to inhibit the process of ox-LDL induced endothelial cell apoptosis, caspase-3 activity, and CHOP mRNA level. Results Ox-LDL treatment significantly increased the expression of PERK, PERK-mediated inactivation of elF2a phosphorylation, and the expression of CHOP, as well as the caspase-3 activity and apoptosis. The effects of ox-LDL were markedly decreased by knocking down PERK with stable transduction of lentiviral shRNA or by selective elF2a phosphatase inhibitor, salubrinal. Conclusion This study provides the first evidence that ox-LDL induces apoptosis in vascular endothelial cells mediated largely via the PERK/elF2a/CHOP ER-stress pathway. It adds new insights into the molecular mechanisms underlying the pathogenesis and progression of atherosclerosis.

关键词： PERK elF2a CHOP Endoplasmic reticulum stress oxidized low-density lipoprotein Endothelial cell Apoptosis Atherosclerosis Caspase-3

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Lectin-like oxidized low-density lipoprotein receptor-1:protein,ligands,expression and pathophvsiological significance

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Chinese Medical Journal 2007年第5期120卷 421-426页

作者： CHEN Xiu-ping DU Guan-hua Institute of Materia Medica Chinese Academy of Medical Sciences and Peking Union Medical College Beijing 100050 China

Objective To review the recent research progress in lectin-like oxidized low-density lipoprotein receptor-1 （LOX-1） including its protein, ligands, expression and pathophysiological significance. Data sources Information included in this article was identified by searching of PUBMED （1997-2006） online resources using the key term LOX-1. Study selection Mainly original milestone articles and critical reviews written by major pioneer investigators of the field were selected. Results The key issues related to the LOX-1 protein as well as ligands for LOX-1. Factors regulating the expression of LOX-1 were summarized. The pathophysiological functions of LOX-1 in several diseases were discussed. Conclusions Identification of LOX-1 and a definition of its biological role in pathophysiologic states provide deeper insight into the pathogenesis of some cardiovascular diseases especially in atherosclerosis and provide a potential selective therapeutic approach. LOX-1 is unlocking and drugs targeting LOX-1 might be a promising direction to explore.

关键词： scavenger receptors, class E oxidized low-density lipoprotein endothelial cells atherosclerosis

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Protective Effect of Propyl Gallate Against oxidized low-density lipoprotein-Induced Injury of Endothelial Cells

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Chinese Journal of Integrative Medicine 2015年第4期21卷 299-306页

作者：马路朱晓法吴育云陈可冀史大卓殷惠军 Department of Geriatric Cardiology the Navy General Hospital of Chinese PLA The Lab of Cardiovascular Molecular Biology Xiyuan HospitalChina Academy of Chinese Medical Sciences

Objective： To evaluate the protective effect of propyl gallate （PG）, an alkyl ester of gallic acid which is an active ingredient of Radix Paeoniae, against oxidized low-density lipoprotein （ox-LDL）-induced apoptosis and death in endothelial cells （ECs） and to find out its preliminary mechanism. Methods： The cultured endothelial cells were divided into normal, model （ox-LDL）, control （fetal bovine serum）, PG high dose （20 p,g/mL）, PG middle dose （10 μg/mL）, and PG low dose （5 μg/mL） groups, each derived from three different pools of umbilical cords. The model of injured human umbilical vein endothelial cells （HUVECs） was induced by ox-LDL. The 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl-2H-tetrazolium bromide （MTT） assay, Hoechst 33258 staining, flow cytometry and measurement of nitrogen monoxidum （NO） release were used to evaluate the protective effect of PG against ox-LDL-induced apoptosis and death in HUVECs. To find out the mechanism of this protective effect, the expression of endothelial nitric oxide synthase （eNOS） mRNA, eNOS protein expression, immunofluorescence of intracellular reactive oxygen species （ROS） and activities of malondialdehyde （MDA）, superoxidedismutase （SOD） and glutathione peroxidase （GPx） were observed. Results： PG significantly reduced ox-LDL-induced apoptosis and cell death. The percentage of cells death and apoptosis was significantly higher in the ox-LDL group than that in the control group （P〈0.05）. Compared with the control group, the cells death and apoptosis of PG group was no different （P〉0.05）. As compared with the ox-LDL group, results of the PG high dose group showed that cell viability was significantly increased （P〈0.05）, the level of NO release, expression of eNOS mRNA, densitometric value of eNOS protein expression, as well as the activities of SOD and GPx were all significantly higher （all P〈0.05）. Conclusion： PG could potentially serve as a novel endothelial protective agent against ox-LDL-induced injury of endothelial cell.

关键词： propyl gallate oxidized low-density lipoprotein endotheliocyte reactive oxygen species Radix Paeoniae Chinese medicine

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Aqueous Extracts of Tribulus terrestris Protects Against oxidized low-density lipoprotein-Induced Endothelial Dysfunction

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Chinese Journal of Integrative Medicine 2016年第3期22卷 193-200页

作者：姜月华杨传华李伟吴赛孟宪卿李东娜 Central Laboratory Affiliated Hospital of Shandong University of Traditional Chinese Medicine Clinical Medical College Shandong University of Traditional Chinese Medicine

Objective： To investigate the role of aqueous extracts of Tribulus terrestris （TT） against oxidized low-density lipoprotein （ox-LDL）-induced human umbilical vein endothelial cells （HUVECs） dysfunction in vitro. Methods： HUVECs were pre-incubated for 60 min with TT （30 and 3 μg/mL respectively） or 105 mol/L valsartan （as positive controls） and then the injured endothelium model was established by applying 100 μg/mL ox-LDL for 24 h. Cell viability of HUVECs was observed by real-time cell electronic sensing assay and apoptosis rate by Annexin V/PI staining. The cell migration assay was performed with a transwell insert system. Cytoskeleton remodeling was observed by immunofluorescence assay. The content of endothelial nitric oxide synthase （eNOS） was measured by enzyme-linked immunosorbent assay. Intracellular reactive oxygen species （ROS） generation was assessed by immunofluorescence and flow cytometer. Key genes associated with the metabolism of ox-LDL were chosen for quantitative real-time polymerase chain reaction to explore the possible mechanism of TT against oxidized LDL-induced endothelial dysfunction. Results： TT suppressed ox-LDL-induced HUVEC proliferation and apoptosis rates significantly （41.1% and 43.5% after treatment for 3 and 38 h, respectively; P〈0.05）. It also prolonged the HUVEC survival time and postponed the cell＇s decaying stage （from the 69th h to over 100 h）. According to the immunofluorescence and transwell insert system assay, TT improved the endothelial cytoskeletal network, and vinculin expression and increased cell migration. Additionally, TT regulated of the synthesis of endothelial nitric oxide synthase and generation of intracellular reactive oxygen species （P〈0.05）. Both 30 and 3μg/mL TT demonstrated similar efficacy to valsartan. TT normalized the increased mRNA expression of PI3Kα and Socs3. It also decreased mRNA expression of Aktl, AMPKα, JAK2, LepR and STAT3 induced by ox-LDL. The most notable changes were JAK2, LepR, PI3Kα, Socs3 and STAT3. Conclusions： TT demonstrated potenti

关键词： Tribulus terrestris human umbilical vein endothelial cells oxidized low-density lipoprotein Chinese herbal medicine

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A modified laser-induced choroidal neovascularization animal model with intravitreal oxidized low-density lipoprotein

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International Journal of Ophthalmology(English edition) 2020年第8期13卷 1187-1194页

作者： Tong Wu Kuan-Rong Dang Ya-Fen Wang Bao-Zhen Lyu Wen-Qin Xu Guo-Rui Dou Jian Zhou Yan-Nian Hui Hong-Jun Du Department of Ophthalmology Xijing HospitalEye Institute of Chinese PLAFourth Military Medical UniversityXi’an 710032Shaanxi ProvinceChina Department of Anatomy and Histology and Embryology Xi’an Health SchoolXi’an 710032Shaanxi ProvinceChina The Orbital Disease Institute of the Third Medical Center of PLA General Hospital Beijing100039China

AIM: To investigate whether intravitreal injection of oxidized low-density lipoprotein(OxLDL) can promote laserinduced choroidal neovascularization(CNV) formation in mice and the mechanism involved, thereby to develop a better animal model.METHODS: C57BL6/J mice were randomized into three groups. Immediately after CNV induction with 532 nm laser photocoagulation, 1.0 μL of OxLDL [100 μg/m L in phosphate-buffered saline(PBS)] was intravitreally injected, whereas PBS and the same volume low-density lipoprotein(LDL;100 μg/m L in PBS) were injected into the vitreous as controls. Angiogenic and inflammatory cytokines were measured by quantitative real-time polymerase chain reaction(q RT-PCR) and Western blotting(WB) after 5 d, and CNV severity was analyzed by choroid flat mount and immunofluorescence staining after 1wk. In vitro, retinal pigment epithelial(RPE) cell line(ARPE19) were treated with OxLDL(LDL as control) for 8 h. Angiogenic and inflammatory cytokine levels were measured. A specific inhibitor of lectin-like oxidized low-density lipoprotein receptor 1(LOX1) was used to evaluate the role of LOX1 in this process.RESULTS: At 7 d after intravitreal injection of 1 μL(100 μg/mL) OxLDL, T15-labeled OxLDL was mainly deposited around the CNV area, and the F4/80-labeled macrophages, the CD31-labeled vascular endothelial cells number and CNV area were increased. Meanwhile, WB and qR T-PCR results showed that vascular endothelial growth factor(VEGF), CC chemokine receptor 2(CCR2), interleukin-6(IL-6), IL-1β, and matrix metalloproteinase 9(MMP9) expressions were increased, which was supported by in vitro experiments in RPE cells. LOX1 inhibitors significantly reduced expressions of inflammatory factors IL-1β and VEGF. CONCLUSION: A modified laser-induced CNV animal model is established with intravitreal injection of 1 μL(100 μg/mL) of OxLDL at 7 d, which at least partially through LOX1. This animal model can be used as a simple model for studying the role of OxLDL in age-related macular degeneration.

关键词： age-related macular degeneration choroidal neovascularization oxidized low-density lipoprotein animal model

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Sulforaphane Attenuates oxidized low-density lipoprotein-induced Platelet Hyper-reactivity through CD36/NOX2-mediated Inhibition of Src/Syk/PKC Signalling Pathway

Sulforaphane Attenuates Oxidized Low-density Lipoprotein-ind...

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中国营养学会第十五届全国营养科学大会

作者：牙甫礼 Weiqi Li Yongjie Ma Dali University

oxidized low-density lipoprotein(oxLDL) potentiates platelet activation in dyslipidemic disorders, which is important in both the early(atherosclerosis) and late(thrombosis) stages of atherothrombosis. Sulforaphane(SFN), a dietary isothiocyanate enriched in cruciferous vegetables, has been shown to exert multiple biological activities, including protection against cardiovascular diseases. The current study sought to investigate the efficacy of SFN on oxLDLinduced platelet reactivity in vitro and the underlying mechanisms. Methods Washed human platelets were pre-incubated with different concentrations of SFN(1, 2.5 or 5 μM) or the vehicle control(0.05% DMSO) for 40 min followed by the addition of oxLDL(50 μg/mL) for additional 20 min. Platelet aggregation, granule secretion and generation of reactive oxygen species(ROS) were determined. In addition, the effect of SFN on phosphorylation of p47, c-Src, Syk, PLCγ2 and PKC were evaluated by Western blotting. Results We found that SFN dose-dependently inhibited human platelet aggregation stimulated by oxLDL in the presence of platelet agonist thrombin. SFN also significantly attenuated oxLDL-stimulated platelet granule secretion, including CD62 P and CD63 expression and PF4 and CCL5 release. Moreover, oxLDL-increased platelet ROS generation that was primarily mediated by NAD phosphate oxidase 2(NOX2) was favourably inhibited by SFN treatment. The phosphorylation of p47, a necessary step in the formation of the active NOX2 complex, was also greatly down-regulated by SFN in oxLDL-treated human platelets. Importantly, SFN did not further decrease platelet p47 phox phosphorylation and ROS generation in the presence of anti-CD36 antibody FA6-152, indicating that CD36 is important for upstream mediating NOX2 activity in the SFN-treated platelets in response to oxLDL. Furthermore, we also found that oxLDLinduced phosphorylation of c-Src, Syk, PLCγ2 and PKC were significantly attenuated by SFN, which was not further decreased in the presence of anti-CD36 antibody FA6-152 or NO

关键词： Sulforaphane oxidized low-density lipoprotein atherothrombosis platelet CD36 NAD phosphate oxidase 2 Src family kinase cardiovascular disease

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Fucoxanthin suppresses OxLDL-induced inflammation via activation of Nrf2 and inhibition of NF-κB signaling

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Asian Pacific Journal of Tropical Biomedicine 2022年第5期12卷 207-215页

作者： Peramaiyan Rajendran Abdullah M AlZahrani Department of Biological Sciences College of ScienceKing Faisal UniversityAl Ahsa 31982Saudi Arabia

Objective:To explore the impact of fucoxanthin on oxidized low-density lipoprotein(OxLDL)-induced stress and inflammation in human endothelial cells and its underlying mechanisms.Methods:HUVECs were treated with OxLDL and/or fucoxanthin for a range of time points and concentrations.We evaluated the effects of fucoxanthin on OxLDL-induced HUVECs using the MTT assay,reactive oxygen species accumulation assay,ELISA,RT-PCR,immunofluorescence,and Western blotting.Results:Fucoxanthin enhanced the cell viability in a dose dependent manner after OxLDL exposure.Furthermore,fucoxanthin pretreatment significantly decreased OxLDL-induced reactive oxygen species production and prevented the activation of the nuclear factor kappa-B pathway,which led to substantial suppression of pro-inflammatory gene expressions.OxLDL-induced upregulation of interleukin-6,intercellular adhesion molecule-1,vascular cell adhesion molecule-1,interleukin-1β,monocyte chemotactic protein-1,cyclooxygenase-1,and tumor necrosis factor-αwas significantly reduced by fucoxanthin.Conclusions:Fucoxanthin can inhibit OxLDL-induced vascular inflammation and oxidative stress in HUVECs by targeting Nrf2 signaling pathways.

关键词： oxidized low-density lipoprotein Fucoxanthin Atherosclerosis Inflammation Oxidative stress Cell viability HUVEC Nrf2 signaling pathway NF-κB

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Atherosclerosis and the Cholesterol Theory: A Reappraisal

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World Journal of Cardiovascular Diseases 2016年第11期6卷 391-409页

作者： Ang Peng Wong Abdul Latiff Mohamed Aleksandra Niedzwiecki Department of Graduate Studies Research and Commercialization Cyberjaya University College of Medical Sciences Cyberjaya Malaysia Dr. Rath Research Institute Santa Clara USA

Atherosclerosis is the precedent to ischemic heart disease, which may lead to angina, myocardial infarct, or heart failure;or to ischemic cerebrovascular disease, which may lead to stroke. The prevailing belief underlying conventional approaches to treatment of atherosclerosis and its sequel is that a diet high in cholesterol and saturated fat is the main contributory factor, triggering cholesterol build up in the intima of the blood vessels. Over the last 60 years, the blame has shifted from fats, to saturated fats, to low-density lipoprotein (LDL), and finally to oxidized LDL (Ox-LDL). Therapy has been predominantly aimed at lowering cholesterol and control of risk factors. However, there is an alternative hypothesis about the cause of heart disease linking it to the weakening of the vascular collagen matrix at the sites of high hemodynamic stress (coronary arteries) which triggers the infiltration of lipoprotein(apo) [Lp(a)] and plaque development. Accordingly, the vascular deposition of large molecules such as Lp(a) and atherosclerosis is the result of the body’s endogenous protective mechanism to reinforce the weakened artery walls. Understanding this mechanism may guide the natural prevention of this disease and form the basis for developing effective therapeutic strategies aiming at natural reversal of atherosclerosis through the reinforcement of the vascular wall structure as its primary goal. This reappraisal of atherosclerosis and the cholesterol theory looked at the historical development of the theory, and the Rath and Pauling unified theory of cardiovascular disease.

关键词： Atherosclerosis low-density lipoprotein oxidized low-density lipoprotein Apolipoprotein

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