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Protective Effect of the Silkworm Protein 30Kc6 on Human Vascular Endothelial Cells Damaged by Oxidized Low Density Lipoprotein (Ox-LDL)  [PDF]
Wei Yu, Huihui Ying, Fudan Tong, Chen Zhang, Yanping Quan, Yaozhou Zhang
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0068746
Abstract: Although the 30K family proteins are important anti-apoptotic molecules in silkworm hemolymph, the underlying mechanism remains to be investigated. This is especially the case in human vascular endothelial cells (HUVECs). In this study, a 30K protein, 30Kc6, was successfully expressed and purified using the Bac-to-Bac baculovirus expression system in silkworm cells. Furthermore, the 30Kc6 expressed in Escherichia coli was used to generate a polyclonal antibody. Western blot analysis revealed that the antibody could react specifically with the purified 30Kc6 expressed in silkworm cells. The In vitro cell apoptosis model of HUVEC that was induced by oxidized low density lipoprotein (Ox-LDL) and in vivo atherosclerosis rabbit model were constructed and were employed to analyze the protective effects of the silkworm protein 30Kc6 on these models. The results demonstrated that the silkworm protein 30Kc6 significantly enhanced the cell viability in HUVEC cells treated with Ox-LDL, decreased the degree of DNA fragmentation and markedly reduced the level of 8-isoprostane. This could be indicative of the silkworm protein 30Kc6 antagonizing the Ox-LDL-induced cell apoptosis by inhibiting the intracellular reactive oxygen species (ROS) generation. Furthermore, Ox-LDL activated the cell mitogen activated protein kinases (MAPK), especially JNK and p38. As demonstrated with Western analysis, 30Kc6 inhibited Ox-LDL-induced cell apoptosis in HUVEC cells by preventing the MAPK signaling pathways. In vivo data have demonstrated that oral feeding of the silkworm protein 30Kc6 dramatically improved the conditions of the atherosclerotic rabbits by decreasing serum levels of total triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and total cholesterol (TC). Furthermore, 30Kc6 alleviated the extent of lesions in aorta and liver in the atherosclerotic rabbits. These data are not only helpful in understanding the anti-apoptotic mechanism of the 30K family proteins, but also provide important information on prevention and treatment of human cardiovascular diseases.
The Induction of Cytokine Release in Monocytes by Electronegative Low-Density Lipoprotein (LDL) Is Related to Its Higher Ceramide Content than Native LDL  [PDF]
Montserrat Estruch,Jose Luis Sanchez-Quesada,Lorea Beloki,Jordi Ordo?ez-Llanos,Sonia Benitez
International Journal of Molecular Sciences , 2013, DOI: 10.3390/ijms14022601
Abstract: Electronegative low-density lipoprotein (LDL(?)) is a minor modified LDL subfraction that is present in blood. LDL(?) promotes inflammation and is associated with the development of atherosclerosis. We previously reported that the increase of cytokine release promoted by this lipoprotein subfraction in monocytes is counteracted by high-density lipoprotein (HDL). HDL also inhibits a phospholipase C-like activity (PLC-like) intrinsic to LDL(?). The aim of this work was to assess whether the inhibition of the PLC-like activity by HDL could decrease the content of ceramide (CER) and diacylglycerol (DAG) generated in LDL(?). This knowledge would allow us to establish a relationship between these compounds and the inflammatory activity of LDL(?). LDL(?) incubated at 37 °C for 20 h increased its PLC-like activity and, subsequently, the amount of CER and DAG. We found that incubating LDL(?) with HDL decreased both products in LDL(?). Native LDL was modified by lipolysis with PLC or by incubation with CER-enriched or DAG-enriched liposomes. The increase of CER in native LDL significantly increased cytokine release, whereas the enrichment in DAG did not show these inflammatory properties. These data point to CER, a resultant product of the PLC-like activity, as a major determinant of the inflammatory activity induced by LDL(?) in monocytes.
Comparison of ox-LDL Levels in Diabetic Patients with Normo-, Micro-, and Macroalbuminuria with Their First Degree Relatives and the Healthy Control Group  [PDF]
Parisa Behzadi,Firouzeh Torabi,Massoud Amini,Ashraf Aminorroaya
International Journal of Endocrinology , 2012, DOI: 10.1155/2012/167154
Abstract: Oxidized low density lipoprotein (ox-LDL) is a product of oxidative stress. In this cross-sectional study, we compared the ox-LDL concentrations in diabetic patients with normoalbuminuria ( ), microalbuminuria ( ), and macroalbuminuria ( ) with their first degree relatives ( ) and healthy control people ( ). They were selected by consecutive patient selection method. The ox-LDL level was assayed using ELISA. We measured blood pressure, lipid profile, fasting plasma glucose (FPG), and HbA1c in all groups. There was no significant difference in ox-LDL concentrations among normoalbuminuric, microalbuminuric, and macroalbuminuric diabetic groups. In diabetic patients with micro- and macroalbuminuria, ox-LDL concentration was higher than their first degree relatives ( and ) and control group ( and , resp.). In normoalbuminuric diabetic persons, ox-LDL concentration was just higher than that of healthy people ( ). There was no statistically significant difference in ox-LDL levels between normoalbuminuric diabetic patients and their first degree relatives. In conclusion, the presence and progression of albuminuria in diabetic patients are not related to ox-LDL concentration and genetic predisposition influences the plasma OX-LDL level. Larger sample size is needed to confirm this conclusion in future studies. 1. Introduction Diabetes mellitus is a common metabolic disease and has been reported as a state of oxidative stress, inflammation, and endothelial dysfunction [1]. One of the ominous complications of this disease is diabetic nephropathy which is a major cause of end stage renal disease worldwide. There are some evidences that oxidative stress is a main culprit of diabetic nephropathy, and increased levels of oxidized low density lipoprotein (ox-LDL) immune complexes were reported in patients with diabetic nephropathy [2]. The oxidative change of LDL affects its clearance and cause cytotoxic and immunogenic effects. We also know that ox-LDL immune-complexes contribute to the development of atherosclerosis [3–5]. However, the results of several researches suggest that ox-LDL contributes to the initiation and progression of diabetic nephropathy. If we consider diabetic nephropathy as sequences of the events, it is starting with endothelial cell dysfunction which is promoted by ox-LDL [6, 7]. Some mechanisms have been expressed to elucidate the effects of ox-LDL on glomerulus. Evidences have been reported that the chemokine cxcl16 is the main receptor in podocyte mediating the uptake of ox-LDL and therefore, initiate a pathologic biochemical pathway which
自制研发奶粉对ox-LDL诱导平滑肌细胞增殖的影响  [PDF]
尹曼
- , 2017, DOI: 10.13982/j.mfst.1673-9078.2017.5.008
Abstract: 研究自制研发的中老年心血管奶粉对氧化型低密度脂蛋白(ox-LDL)诱导的平滑肌细胞增殖与NO释放量的影响。用ox-LDL诱导血管平滑肌细胞(vascular smooth muscle cell,VSMC)增殖,建立VSMC增殖模型,通过比较自制奶粉与3种常见市售奶粉对模型细胞的增殖抑制作用和NO释放量的数据结果,评价实验室自制研发奶粉的功效。结果表明,30 μg/mL的ox-LDL作用VSMC 24 h可极显著的促进细胞增殖并抑制NO的释放(p<0.01),说明模型构建成功;在此VSMC增殖模型中分别添加奶粉样品,得出自制奶粉在200、400、800 μg/mL均能抑制ox-LDL诱导的VSMC的增殖,且在400 μg/mL的抑制作用极显著(p<0.01),并均能极显著的促进NO的释放(p<0.01)。说明自制研发的中老年心血管奶粉能够抑制ox-LDL诱导的VSMC增殖模型,具有较好的预防动脉粥样硬化的功效。
The effect of self-developed milk powder on the proliferation and nitric oxide (NO) production of vascular smooth muscle cells (VSMC) induced by oxidized-low density lipoprotein (ox-LDL) was studied. A VSMC proliferation model was established by inducing the proliferation of VSMC with ox-LDL. The effects of the milk powder developed in our laboratory was evaluated by comparing its inhibitory effect on the proliferation and NO production of the model cells with three kinds of common commercial milk powders. The results indicated that when VSMCs were treated with 30 μg/mL ox-LDL for 24 h, cell proliferation was significantly promoted and NO release was inhibited (p<0.01), indicating that the model was successfully established. In this VSMC model, different amounts of self-developed milk powder were added, and the results showed that solutions of 200, 400, and 800 μg/mL milk powder inhibited ox-LDL-induced VSMC proliferation. In addition, 400 μg/mL milk powder highly inhibited cell proliferation and promoted NO production (p<0.01). The above findings demonstrate that self-developed milk powder inhibited the ox-LDL-induced proliferation in VSMCs; therefore these milk powders may prevent atherosclerosis and be beneficial for middle-aged and older populations.
Induction of macrophage inflammatory cytokines by Ox-LDL is ABCA1 dependent

Zhi-Gang Guo,Jian-Hua Li,Di Xie,Wen-Yan Lai,Jia-Yi Wu,Ping-Sheng Wu,

老年心脏病学杂志(英文版) , 2010,
Abstract: Objective The current study aimed to evaluate whether the induction of macrophage inflammatory cytokines by Ox-LDL is related to the expression of ABCA1 pathway. Methods After THP1/PMA macrophages were transfected with ABCA1 antisense oligonucleotides (100nmol/L) followed by treatment with Ox-LDL (30mg/L), the expressions of ABCA1, ICAM-1 and MCP-1 mRNA and protein were determined by real-time fluorescent quantitative RT-PCR, Western blot or ELISA. Results Ox-LDL induced expressions of ABCA1, ICAM-1, and MCP-1 at both mRNA and protein levels from THP1/PMA macrophages. Transfection with ABCA1 antisense oligonucleotides reduced ABCA1 mRNA levels after 3 and 6 hours and protein levels after 12 and 24 hours. The expression of ICAM-1 and MCP-1 induced by Ox-LDL was also decreased after inhibition of ABCA1 protein expression by ABCA1 antisense oligonucleotide decreased. Conclusion The induction of macrophage inflammatory cytokines by Ox-LDL is partially dependent on expression of ABCA1. Our studies disclose new functions of ABCA1 in macrophages (J Geriatr Cardiol 2010; 7:166-170).
Induction of macrophage inflammatory cytokines by Ox-LDL is ABCA1 dependent
Zhi-Gang Guo,Jian-Hua Li,Di Xie,Wen-Yan Lai
老年心脏病学杂志(英文版) , 2010,
Abstract: Objective The current study aimed to evaluate whether the induction of macrophage inflammatory cytokines by Ox-LDL is related to the expression of ABCA1 pathway. Methods After THP1/PMA macrophages were transfected with ABCA1 antisense oligonucleotides (100 nmol/L) followed by treatment with Ox-LDL (30 mg/L), the expressions of ABCA1, ICAM-1 and MCP-1 mRNA and protein were determined by real-time fluorescent quantitative RT-PCR, Western blot or ELISA. Results Ox-LDL induced expressions of ABCA1, ICAM-1, and MCP-1 at both mRNA and protein levels from THP1/PMA macrophages. Transfection with ABCA1 antisense oligonucleotides reduced ABCA1 mRNA levels after 3 and 6 hours and protein levels after 12 and 24 hours. The expression of ICAM-1 and MCP-1 induced by Ox-LDL was also decreased after inhibition of ABCA1 protein expression by ABCA1 antisense oligonucleotide decreased. Conclusion The induction of macrophage inflammatory cytokines by Ox-LDL is partially dependent on expression of ABCA1. Our studies disclose new functions of ABCA1 in macrophages.
Effects of Ox-LDL on Macrophages NAD(P)H Autofluorescence Changes by Two-photon Microscopy  [PDF]
Ching-Ting Lin,En-Kuang Tien,Szu-Yuan Lee,Long-Sheng Lu,Chau-Chung Wu,Chen-Yuan Dong,Chii-Wann Lin
Physics , 2007,
Abstract: Ox-LDL uptakes by macrophage play a critical role in the happening of atherosclerosis. Because of its low damage on observed cells and better signal-to- background ratio, two-photon excitation fluorescence microscopy is used to observe NAD(P)H autofluorescence of macrophage under difference cultured conditions- bare cover glass, coated with fibronectin or poly-D-lysine. The results show that the optimal condition is fibronectin coated surface, on which, macrophages profile can be clearly identified on NAD(P)H autofluorescence images collected by two-photon microscopy. Moreover, different morphology and intensities of autofluorescence under different conditions were observed as well. In the future, effects of ox-LDL on macrophages will be investigated by purposed system to research etiology of atherosclerosis.
Effect of immunization against ox-LDL with two different antigens on formation and development of atherosclerosis
Sedigheh Asgary, Salb-Ali Saberi, Shirin Azampanah
Lipids in Health and Disease , 2007, DOI: 10.1186/1476-511x-6-32
Abstract: LDL was isolated from hypercholesterolemic rabbits plasma and oxidized with MDA or Cu++. Rabbits were divided to three groups and immunized with MDA-LDL or Cu-LDL or phosphate-buffer (PBS) as a control group. Immunization was repeated after 2, 4, 6, and 8 weeks and concentration of antibodies against ox-LDL was measured in each stage. After immunization, rabbits in each group were divided to two subgroups based on the dietary regimen (fed normal or high cholesterol diet). At the beginning and the end of the study, biochemical factors were measured. Also, fatty streaks in aorta and left and right coronary arteries evaluated.Immunization with Cu2+-LDL and MDA-LDL induced statistically significant antibodies against ox-LDL. In hypercholesterolemic rabbits immunized with MDA-LDL the level of cholesterol, LDL-cholesterol, triglyceride, fasting blood sugar and fatty streak lesions in aorta and right coronary arteries were significantly decreased as compared with non-immunized high-cholesterol group. Immunization with Cu2+-LDL in hypercholesterolemic rabbits significantly decreased triglyceride, fasting blood sugar, cholesterol and CRP. No significant differences were detected in the fatty streak lesions in this group as compared with non-immunized high-cholesterol diet. In groups under normal diet immunized with MDA-LDL or Cu2+-LDL no significant effect on biochemical factors and atherosclerotic lesions were observed.This study indicates that although the effect of produced antibodies in several methods and different dietary regimens is different, immunization against ox-LDL is antiatherogenic.In the recent studies, relation between immune system and atherosclerosis has been investigated [1-3]. It is clear that this system can be effective on severity of atherosclerosis through different immunogenic mechanisms [4-6]. Several studies were pointed to oxidized LDL (ox-LDL) as one of the main immunogenes which have important roles in primary lesions of atherosclerosis [5,6].
Inflammation Disrupts the LDL Receptor Pathway and Accelerates the Progression of Vascular Calcification in ESRD Patients  [PDF]
Jing Liu, Kun Ling Ma, Min Gao, Chang Xian Wang, Jie Ni, Yang Zhang, Xiao Liang Zhang, Hong Liu, Yan Li Wang, Bi Cheng Liu
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047217
Abstract: Background Chronic inflammation plays a crucial role in the progression of vascular calcification (VC). This study was designed to investigate whether the low-density lipoprotein receptor (LDLr) pathway is involved in the progression of VC in patients with end-stage renal disease (ESRD) during inflammation. Methods and Results Twenty-eight ESRD patients were divided into control and inflamed groups according to plasma C-reactive protein (CRP) level. Surgically removed tissues from the radial arteries of patients receiving arteriovenostomy were used in the experiments. The expression of tumour necrosis factor-α (TNF-α) and monocyte chemotactic protein-1 (MCP-1) of the radial artery were increased in the inflamed group. Hematoxylin-eosin and alizarin red S staining revealed parallel increases in foam cell formation and calcium deposit formation in continuous cross-sections of radial arteries in the inflamed group compared to the control, which were closely correlated with increased LDLr, sterol regulatory element binding protein-2 (SREBP-2), bone morphogenetic proteins-2 (BMP-2), and collagen I protein expression, as shown by immunohistochemical and immunofluorescent staining. Confocal microscopy confirmed that inflammation enhanced the translocation of the SREBP cleavage-activating protein (SCAP)/SREBP-2 complex from the endoplasmic reticulum to the Golgi, thereby activating LDLr gene transcription. Inflammation increased alkaline phosphatase protein expression and reduced α-smooth muscle actin protein expression, contributing to the conversion of the vascular smooth muscle cells in calcified vessels from the fibroblastic to the osteogenic phenotype; osteogenic cells are the main cellular components involved in VC. Further analysis showed that the inflammation-induced disruption of the LDLr pathway was significantly associated with enhanced BMP-2 and collagen I expression. Conclusions Inflammation accelerated the progression of VC in ESRD patients by disrupting the LDLr pathway, which may represent a novel mechanism involved in the progression of both VC and atherosclerosis.
不同浓度ox-LDL对大鼠原代卵泡膜细胞增殖及激素合成相关基因LXR-α和StAR表达的影响
Effects of different concentrations of ox-LDL on the proliferation of rat theca cells and the expression of steroidogenesis related genes LXR-α and StAR
 [PDF]

陈莹,张益,李聪
CHEN Ying
, ZHANG Yi, LI Cong

- , 2017, DOI: 10.3969/j.issn.1674-8115.2017.03.008
Abstract: 目的 ·初步探讨ox-LDL对大鼠卵泡膜细胞增殖和雄激素合成相关基因LXR-α和StAR表达的影响。方法 ·免疫组化检测大鼠卵巢组织中LXR-α的表达。体外分离培养原代大鼠卵泡膜细胞,分别用25、50、100、150、200、300和400 mg/L的ox-LDL处理,用real-time PCR检测LXR-α mRNA的变化,用MTT检测细胞活力,用Western blotting检测LXR-α和StAR蛋白的表达。结果 · ox-LDL对大鼠卵泡膜细胞增殖的影响和对LXR-α和StAR表达的调控呈现浓度依赖性变化。ox-LDL刺激24 h后,低浓度的ox-LDL(25~150 mg/L)可诱导卵泡膜细胞增殖,以100 mg/L的ox-LDL对卵泡膜细胞增殖的促进作用显著。而当ox-LDL浓度继续上升,细胞存活率下降,以400 mg/L的ox-LDL对卵泡膜细胞增殖的抑制作用显著。低浓度ox-LDL(25~150 mg/L)刺激,导致LXR-α mRNA的表达升高,其中150 mg/L ox-LDL对LXR-α mRNA的表达量影响显著。高浓度ox-LDL抑制LXR-α mRNA的表达,其中400 mg/L的ox-LDL对LXR-α mRNA的表达量影响显著。150 mg/L ox-LDL促进大鼠卵泡膜细胞LXR-α和StAR蛋白的表达上升,但150 mg/L ox-LDL对StAR蛋白表达的促进作用,与对照组相比,差异没有统计学意义;而400 mg/L ox-LDL能显著抑制大鼠卵泡膜细胞LXR-α和StAR蛋白的表达。结论 ·低浓度的ox-LDL可诱导卵泡膜细胞增殖,促进LXR-α和StAR的表达,而高浓度oxLDL降低细胞活力,抑制LXR-α和StAR的表达。
: Objective · To investigate the effects of ox-LDL on the proliferation of rat theca cells and expression of LXR-α and StAR, two genes associated with androgen biosynthesis. Methods · The expression of LXR-α in the ovarian tissue of rats was determined by immunohistochemistry. Primary theca cells were isolated and collected from rat ovary and cultured in vitro. Furthermore, the theca cells were treated with 25, 50, 100, 150, 200, 300 and 400 mg/L ox-LDL,respectively. The variations in LXR-α mRNA were identified using real-time PCR. MTT assay was performed to detect cell viability. The expression of LXR-α and StAR was measured by Western blotting analysis. Results · The effect of ox-LDL on the proliferation of rat theca cells and the levels of LXR-α and StAR in theca cells was in a concentration-dependent manner. Following exposure to various concentration of ox-LDL for 24 h, the proliferation of theca cells was induced by low concentration of ox-LDL (25-150 mg/L), and 100 mg/L ox-LDL showed the most significant inducing effect. Moreover, the cell survival rate was diminished considerably following with ox-LDL concentration increasing, especially lowered by 400 mg/L ox-LDL. The mRNA level of LXR-α was increased with low concentration of ox-LDL (25-150 mg/L) and the impact of ox-LDL on the induced expression of LXR-α mRNA was considerably distinct at the concentration of 150 mg/L. On the other hand, the expression of LXR-α mRNA was reduced with high concentration of ox-LDL, and the impact of 400 mg/L ox-LDLwas substantially distinct. The protein expression levels of LXR-α and StAR were increased with 150 mg/L ox-LDL, but StAR protein level in 150 mg/L ox-LDL group revealed no significant difference when compared with control group. The expression of LXR-α and StAR protein was significantly inhibited with 400 mg/L
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