Search

Your search keyword '"Chen, Yan"' showing total 6 results
Start Over Author "Chen, Yan" Topic atherosclerosis Topic inflammation
6 results on '"Chen, Yan"'

1. Activation of the CXCL16/CXCR6 Pathway by Inflammation Contributes to Atherosclerosis in Patients with End-stage Renal Disease.

Author

Hu ZB, Chen Y, Gong YX, Gao M, Zhang Y, Wang GH, Tang RN, Liu H, Liu BC, and Ma KL

Subjects
ADAM10 Protein metabolism, Adult, Aged, Amyloid Precursor Protein Secretases metabolism, Atherosclerosis metabolism, Chemokine CCL2 metabolism, Chemokine CXCL16, Chemokines, CXC genetics, Female, Humans, Inflammation metabolism, Kidney Failure, Chronic metabolism, Male, Membrane Proteins metabolism, Middle Aged, Receptors, CXCR6, Receptors, Chemokine genetics, Receptors, Purinergic P2X7 metabolism, Receptors, Scavenger genetics, Receptors, Virus genetics, Tumor Necrosis Factor-alpha metabolism, Atherosclerosis etiology, Chemokines, CXC metabolism, Inflammation complications, Kidney Failure, Chronic complications, Receptors, Chemokine metabolism, Receptors, Scavenger metabolism, Receptors, Virus metabolism
Abstract

Background: Chronic inflammation plays a critical role in the progression of atherosclerosis (AS). This study aimed to determine the effects of the CXC chemokine ligand 16 (CXCL16)/CXC chemokine receptor 6 (CXCR6) pathway on cholesterol accumulation in the radial arteries of end-stage renal disease (ESRD) patients with concomitant microinflammation and to further investigate the potential effects of the purinergic receptor P2X ligand-gated ion channel 7 (P2X7R). Methods: Forty-three ESRD patients were divided into the control group (n=17) and the inflamed group (n=26) based on plasma C-reactive protein (CRP) levels. Biochemical indexes and lipid profiles of the patients were determined. Surgically removed tissues from the radial arteries of patients receiving arteriovenostomy were used for preliminary evaluation of AS. Haematoxylin-eosin (HE) and Filipin staining were performed to assess foam cell formation. CXCL16/CXCR6 pathway-related protein expression, P2X7R protein expression and the expression of monocyte chemotactic protein-1 (MCP-1), tumour necrosis factor-α (TNF-α), and CD68 were detected by immunohistochemical and immunofluorescence staining. Results: Inflammation increased both MCP-1 and TNF-α expression and macrophage infiltration in radial arteries. Additionally, foam cell formation significantly increased in the radial arteries of the inflamed group compared to that of the controls. Further analysis showed that protein expression of CXCL16, CXCR6, disintegrin and metalloproteinase-10 (ADAM10) in the radial arteries of the inflamed group was significantly increased. Furthermore, CXCL16 expression was positively correlated with P2X7R expression in the radial arteries of ESRD patients. Conclusions: Inflammation contributed to foam cell formation in the radial arteries of ESRD patients via activation of the CXCL16/CXCR6 pathway, which may be regulated by P2X7R., Competing Interests: The authors have declared that no competing interest exists.

Published
2016
Full Text
View/download PDF

2. Analysis of Immune and Inflammation Characteristics of Atherosclerosis from Different Sample Sources

Author

HAN NIE, Chen Yan, Weimin Zhou, and Tao-sheng Li

Subjects
Carotid Artery Diseases, Inflammation, Aging, Article Subject, animal diseases, Computational Biology, chemical and pharmacologic phenomena, Cell Biology, General Medicine, biochemical phenomena, metabolism, and nutrition, Atherosclerosis, Biochemistry, Plaque, Atherosclerotic, Cardiovascular Diseases, bacteria, Humans, Gene Regulatory Networks
Abstract

Background: Atherosclerosis is the predominant cause of cardiovascular diseases. Existing studies suggest that the development of atherosclerosis is closely related to inflammation and immunity, but whether there are differences and similarities between atherosclerosis occurring at different sites is still unknown. We elucidated the pathological characteristics of peripheral vascular diseases by using bioinformatic analyses on immune cells and inflammation-related gene expression in atherosclerotic arteries and plaques. Methods: Eight data sets regarding atherosclerosis were downloaded from the Gene Expression Omnibus database. Human immune genes were obtained from the IMMPORT website. The samples were scored and divided into highand low-immune groups. Then the samples were analysed using weighted gene co-expression network analysis, while the modules were analysed using functional enrichment. The protein–protein interaction network was constructed using the STRING and Cytoscape databases. The hub immune genes were screened, and the correlation between hub immune genes and immune cells was analysed. Results: Immune cells and their functions were significantly different during atherosclerosis development. The infiltration proportion of immune cells was approximately similar in samples from different sources of patients with carotid atherosclerosis. However, the sensitivity of lower extremity atherosclerosis samples to immune cells is lower than that of carotid atherosclerosis samples.The samples from the plaque and artery were mainly infiltrated by macrophages, T cells and mast cells. After immune cells were assessed, resting NK cells, activated mast cells and M0 macrophages were found to be key immune cells in atherosclerosis and plaque formation. In addition, CCL4, TLR2, IL1B and PTPRC were considered to be immune marker genes in atherosclerosis development. Conclusion: Bioinformatic data analysis confirms the essential role of immune cells in cardiovascular diseases, and also indicates some differences of immune and inflammation characteristics of atherosclerosis between carotid and lower extremity arteries., Oxidative medicine and cellular longevity, 2022, art. no. 5491038; 2022

Published
2021

3. Discovery, synthesis and anti-atherosclerotic activities of a novel selective sphingomyelin synthase 2 inhibitor

Author

Qi Xiangyu, Huiti Li, Tingbo Ding, Jibin Dong, Chen Yan, Min Wei, Shuang Hu, Yang Cao, Nengneng Cheng, Li Yali, Mo Mingguang, Bin Lou, Deyong Ye, Yong Chu, Xiaoxia Li, Xian-Cheng Jiang, Taomin Huang, and Lu Zhou

Subjects
Chemokine, Apolipoprotein B, medicine.medical_treatment, Transferases (Other Substituted Phosphate Groups), Pharmacology, 01 natural sciences, Cell Line, Mice, 03 medical and health sciences, Apolipoproteins E, Pharmacokinetics, Drug Discovery, medicine, Animals, Homeostasis, Humans, Macrophage, Secretion, 030304 developmental biology, Inflammation, Mice, Knockout, 0303 health sciences, biology, 010405 organic chemistry, Chemistry, Macrophages, Organic Chemistry, General Medicine, Atherosclerosis, Lipid Metabolism, 0104 chemical sciences, Cytokine, Benzamides, Knockout mouse, biology.protein, Efflux
Abstract

The sphingomyelin synthase 2 (SMS2) is a potential target for pharmacological intervention in atherosclerosis. However, so far, few selective SMS2 inhibitors and their pharmacological activities were reported. In this study, a class of 2-benzyloxybenzamides were discovered as novel SMS2 inhibitors through scaffold hopping and structural optimization. Among them, Ly93 as one of the most potent inhibitors exhibited IC50 values of 91 nM and 133.9 μM against purified SMS2 and SMS1 respectively. The selectivity ratio of Ly93 was more than 1400-fold for purified SMS2 over SMS1. The in vitro studies indicated that Ly93 not only dose-dependently diminished apoB secretion from Huh7 cells, but also significantly reduced the SMS activity and increased cholesterol efflux from macrophages. Meanwhile, Ly93 inhibited the secretion of LPS-mediated pro-inflammatory cytokine and chemokine in macrophages. The pharmacokinetic profiles of Ly93 performed on C57BL/6J mice demonstrated that Ly93 was orally efficacious. As a potent selective SMS2 inhibitor, Ly93 significantly decreased the plasma SM levels of C57BL/6J mice. Furthermore, Ly93 was capable of dose-dependently attenuating the atherosclerotic lesions in the root and the entire aorta as well as macrophage content in lesions, in apolipoprotein E gene knockout mice treated with Ly93. In conclusion, we discovered a novel selective SMS2 inhibitor Ly93 and demonstrated its anti-atherosclerotic activities in vivo. The preliminary molecular mechanism-of-action studies revealed its function in lipid homeostasis and inflammation process, which indicated that the selective inhibition of SMS2 would be a promising treatment for atherosclerosis.

Published
2019

4. The role of pro-inflammatory cytokines in lipid metabolism of metabolic diseases.

Author

Chen, Yan, Yu, Chun-Yan, and Deng, Wei-Min

Subjects
*LIPID metabolism, *METABOLIC disorders, *LIPID synthesis, *CYTOKINES, *BLOOD lipids, *INFLAMMATION, *CANCER, *ATHEROSCLEROSIS, *FATTY liver
Abstract

Adipose tissue has been considered as a crucial source of certain pro-inflammatory cytokines; conversely, these pro-inflammatory cytokines are involved in regulating the proliferation and apoptosis of adipocytes, promoting lipolysis, inhibiting lipid synthesis and decreasing blood lipids, etc. In recent decades, extensive studies have indicated that pro-inflammatory cytokines play important roles in the development of lipid metabolism of metabolic diseases, including obesity, atherosclerosis, steatohepatitis and hyperlipoproteinemia. However, the involved pro-inflammatory cytokines types and the underlying mechanisms remain largely unknown. The "re-discovery" of cancer as a metabolic disorder largely occurred in the last five years. Although pro-inflammatory cytokines have been intensively investigated in cancer research, there are very few studies about the roles of pro-inflammatory cytokines in the lipid metabolism of cancer. In the current review, we provide an overview of the progress that has been made in the roles of different pro-inflammatory cytokines in lipid metabolism of metabolic diseases including cancer. [ABSTRACT FROM AUTHOR]

Published
2019
Full Text
View/download PDF

5. Vinpocetine Attenuates Lipid Accumulation and Atherosclerosis Formation

Author

Chen Yan, Yu-Jun Cai, and Jian Dong Li

Subjects
Apolipoprotein E, Biophysics, Fluorescent Antibody Technique, Inflammation, Pharmacology, Biology, Biochemistry, Article, Cell Line, chemistry.chemical_compound, Mice, Vinpocetine, medicine, Animals, Scavenger receptor, Molecular Biology, Vinca Alkaloids, Foam cell, Mice, Knockout, Cholesterol, Macrophages, Cell Biology, Arteriosclerosis, medicine.disease, Atherosclerosis, Lipid Metabolism, Scavenger Receptors, Class E, Dietary Fats, Lipoproteins, LDL, chemistry, Immunology, lipids (amino acids, peptides, and proteins), medicine.symptom, medicine.drug, Lipoprotein
Abstract

Atherosclerosis, the major cause of myocardial infarction and stroke, is a chronic arterial disease characterized by lipid deposition and inflammation in the vessel wall. Cholesterol, in low-density lipoprotein (LDL), plays a critical role in the pathogenesis of atherosclerosis. Vinpocetine, a derivative of the alkaloid vincamine, has long been used as a cerebral blood flow enhancer for treating cognitive impairment. Recent study indicated that vinpocetine is a potent anti-inflammatory agent. However, its role in the pathogenesis of atherosclerosis remains unexplored. In the present study, we show that vinpocetine significantly reduced atherosclerotic lesion formation in ApoE knockout mice fed with a high-fat diet. In cultured murine macrophage RAW264.7 cells, vinpocetine markedly attenuated oxidized LDL (ox-LDL) uptake and foam cell formation. Moreover, vinpocetine greatly blocked the induction of ox-LDL receptor 1 (LOX-1) in cultured macrophages as well as in the LOX-1 level in atherosclerotic lesions. Taken together, our data reveal a novel role of vinpocetine in reduction of pathogenesis of atherosclerosis, at least partially through suppressing LOX-1 signaling pathway. Given the excellent safety profile of vinpocetine, this study suggests vinpocetine may be a therapeutic candidate for treating atherosclerosis.

Published
2013

6. Viflpocetine inhibits NF-κB–dependent inflammation via an IKK-dependent but PDE-independent mechanism.

Author

Kye-Im Jeon, Xiangbin Xu, Aizawa, Toru, Jae Hyang Lim, Hirofumi Jono, Dong-Seok Kwon, Jun-ichi Abe, Berk, Bradford C., Jian-Dong Li, and Chen Yan

Subjects
INFLAMMATION, ATHEROSCLEROSIS, VINPOCETINE, ANTI-inflammatory agents, OBSTRUCTIVE lung diseases, EPITHELIAL cells
Abstract

Inflammation is a hallmark of many diseases, such as atherosclerosis, chronic obstructive pulmonary disease, arthritis, infectious diseases, and cancer. Although steroids and cyclooxygenase inhibitors are effective antiinflammatory therapeutical agents, they may cause serious side effects. Therefore, developing unique antiinflammatory agents without significant adverse effects is urgently needed. Vinpocetine, a derivative of the alkaloid vincamine, has long been used for cerebrovascular disorders and cognitive impairment Its role in inhibiting inflammation, however, remains unexplored. Here, we show that vinpocetine acts as an antiinflammatory agent in vitro and in vivo. In particular, vinpocetine inhibits TNF-α-induced NF-κB activation and the subsequent induction of proinflammatory mediators in multiple cell types, including vascular smooth muscle cells, endothelial cells, macrophages, and epithelial cells. We also show that vinpocetine inhibits monocyte adhesion and chemotaxis, which are critical processes during inflammation. Moreover, vinpocetine potently inhibits TNF-α- or LPS-induced up-regulation of proinflammatory mediators, including TNF-α, lL-1β, and macrophage inflammatory protein-2, and decreases interstitial infiltration of polymorphonuclear leukocytes in a mouse model of TNF-α- or LPSinduced lung inflammation. Interestingly, vinpocetine inhibits NF-κB-dependent inflammatory responses by directly targeting IKK, independent of its well-known inhibitory effects on phosphodiesterase and Ca2+ regulation. These studies thus identify vinpocetine as a unique antiinflammatory agent that may be repositioned for the treatment of many inflammatory diseases. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results