Publications by authors named "Wen-Yi Deng"

7 Publications

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Biochanin A Mitigates Atherosclerosis by Inhibiting Lipid Accumulation and Inflammatory Response.

Oxid Med Cell Longev 2020 11;2020:8965047. Epub 2020 Nov 11.

Department of Pathophysiology, School of Basic Medical Sciences, Anhui Medical University, Hefei, 230032 Anhui, China.

Biochanin A (BCA), a dietary isoflavone extracted from red clover and cabbage, has been shown to antagonize hypertension and myocardial ischemia/reperfusion injury. However, very little is known about its role in atherogenesis. The aim of this study was to observe the effects of BCA on atherosclerosis and explore the underlying mechanisms. Our results showed that administration of BCA promoted reverse cholesterol transport (RCT), improved plasma lipid profile, and decreased serum proinflammatory cytokine levels and atherosclerotic lesion area in apoE mice fed a Western diet. In THP-1 macrophage-derived foam cells, treatment with BCA upregulated ATP-binding cassette (ABC) transporter A1 (ABCA1) and ABCG1 expression and facilitated subsequent cholesterol efflux and diminished intracellular cholesterol contents by activating the peroxisome proliferator-activated receptor (PPAR)/liver X receptor (LXR) and PPAR/heme oxygenase 1 (HO-1) pathways. BCA also activated these two signaling pathways to inhibit the secretion of proinflammatory cytokines. Taken together, these findings suggest that BCA is protective against atherosclerosis by inhibiting lipid accumulation and inflammatory response through the PPAR/LXR and PPAR/HO-1 pathways. BCA may be an attractive drug for the prevention and treatment of atherosclerotic cardiovascular disease.
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http://dx.doi.org/10.1155/2020/8965047DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8074550PMC
May 2021

CTRP12 ameliorates atherosclerosis by promoting cholesterol efflux and inhibiting inflammatory response via the miR-155-5p/LXRα pathway.

Cell Death Dis 2021 Mar 10;12(3):254. Epub 2021 Mar 10.

Institute of Clinical Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570100, Hainan, China.

C1q tumor necrosis factor-related protein 12 (CTRP12), a conserved paralog of adiponectin, is closely associated with cardiovascular disease. However, little is known about its role in atherogenesis. The aim of this study was to examine the influence of CTRP12 on atherosclerosis and explore the underlying mechanisms. Our results showed that lentivirus-mediated CTRP12 overexpression inhibited lipid accumulation and inflammatory response in lipid-laden macrophages. Mechanistically, CTRP12 decreased miR-155-5p levels and then increased its target gene liver X receptor α (LXRα) expression, which increased ATP binding cassette transporter A1 (ABCA1)- and ABCG1-dependent cholesterol efflux and promoted macrophage polarization to the M2 phenotype. Injection of lentiviral vector expressing CTRP12 decreased atherosclerotic lesion area, elevated plasma high-density lipoprotein cholesterol levels, promoted reverse cholesterol transport (RCT), and alleviated inflammatory response in apolipoprotein E-deficient (apoE) mice fed a Western diet. Similar to the findings of in vitro experiments, CTRP12 overexpression diminished miR-155-5p levels but increased LXRα, ABCA1, and ABCG1 expression in the aortas of apoE mice. Taken together, these results suggest that CTRP12 protects against atherosclerosis by enhancing RCT efficiency and mitigating vascular inflammation via the miR-155-5p/LXRα pathway. Stimulating CTRP12 production could be a novel approach for reducing atherosclerosis.
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http://dx.doi.org/10.1038/s41419-021-03544-8DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7947013PMC
March 2021

Kidney xenotransplantation: Recent progress in preclinical research.

Clin Chim Acta 2021 Mar 7;514:15-23. Epub 2020 Dec 7.

Institute of Clinical Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan 460106, China; Department of Organ Transplantation, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan 460106, China; The Transplantation Institute of Hainan Medical University, Haikou, Hainan 460106, China. Electronic address:

Kidney transplantation is the most effective treatment for end-stage renal disease, but is limited by the increasing shortage of deceased and living human donor kidneys. Xenotransplantation using pig organs provides the possibility to resolve the issue of organ supply shortage and is regarded as the next great medical revolution. In the past five years, there have been sequential advances toward the prolongation of life-supporting pig kidney xenograft survival in non-human primates, with the longest survival being 499 days. This progress is due to the growing availability of pigs with multi-layered genetic modifications to overcome the pathobiological barriers and the application of a costimulation blockade-based immunosuppressive regimen. These encouraging results bring the hope to initiate the clinical trials of pig kidney transplantation in the near future. In this review, we summarized the latest advances regarding pig kidney xenotransplantation in preclinical models to provide a basis for future investigation and potential clinical translation.
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http://dx.doi.org/10.1016/j.cca.2020.11.028DOI Listing
March 2021

LncRNA kcnq1ot1 promotes lipid accumulation and accelerates atherosclerosis via functioning as a ceRNA through the miR-452-3p/HDAC3/ABCA1 axis.

Cell Death Dis 2020 12 9;11(12):1043. Epub 2020 Dec 9.

Institute of Clinical Medicine, The Second Affiliated Hospital of Hainan Medical University, Haikou, 570100, Hainan, PR China.

Kcnq1 overlapping transcript 1 (kcnq1ot1), an imprinted antisense lncRNA in the kcnq1 locus, acts as a potential contributor to cardiovascular disease, but its role in atherosclerosis remains unknown. The aim of this study was to explore the effects of kcnq1ot1 on atherogenesis and the underlying mechanism. Our results showed that kcnq1ot1 expression was significantly increased in mouse aorta with atherosclerosis and lipid-loaded macrophages. Lentivirus-mediated kcnq1ot1 overexpression markedly increased atherosclerotic plaque area and decreased plasma HDL-C levels and RCT efficiency in apoE mice fed a Western diet. Upregulation of kcnq1ot1 also reduced the expression of miR-452-3p and ABCA1 but increased HDAC3 levels in mouse aorta and THP-1 macrophages. Accordingly, kcnq1ot1 overexpression inhibited cholesterol efflux and promoted lipid accumulation in THP-1 macrophages. In contrast, kcnq1ot1 knockdown protected against atherosclerosis in apoE mice and suppressed lipid accumulation in THP-1 macrophages. Mechanistically, kcnq1ot1 enhanced HDAC3 expression by competitively binding to miR-452-3p, thereby inhibiting ABCA1 expression and subsequent cholesterol efflux. Taken together, these findings suggest that kcnq1ot1 promotes macrophage lipid accumulation and accelerates the development of atherosclerosis through the miR-452-3p/HDAC3/ABCA1 pathway.
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http://dx.doi.org/10.1038/s41419-020-03263-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7723992PMC
December 2020

Effect of calcium oxide (CaO) and sawdust on adhesion and cohesion characteristics of sewage sludge under agitated and non-agitated drying conditions.

Water Res 2017 03 2;110:150-160. Epub 2016 Dec 2.

School of Environmental Science and Engineering, Donghua University, Shanghai 201620, China.

Stickiness phenomenon is widely observed in sewage sludge drying practices. This paper is aimed at demonstrating and comparing the sticky properties of sewage sludge through non-agitated and agitated drying tests specially designed for sewage sludge. Special attentions were paid to the effects of additives, i.e. CaO, fine sawdust (FSD) and coarse sawdust (CSD), on the adhesive and cohesive characteristics of sewage sludge. The results indicated that the sticky properties of the sludge were markedly different under the different testing methods, and was also greatly influenced by CaO or sawdust addition. For instance, in the non-agitated drying tests, CaO can significantly enhance the maximum adhesive and cohesive stresses of the sludge, whereas in the agitated drying tests, the torque of agitation, which strongly correlated with the cohesive stress of the sludge, was lowered by CaO addition. During agitated drying process, sludge lump with CaO addition started to break up at higher moisture content than that of original sludge. On the other hand, sawdust also affected the sticky properties of sludge in a way that was totally different with CaO. After sawdust addition (at 5-10%WS (wet sludge basis)), the cohesive stress of the sludge was markedly increased due to strengthening of mechanical interlocking inside the sludge, whereas the adhesiveness of the sludge was lowered by sawdust addition. The influencing mechanisms of CaO and sawdust under the different testing methods were detailedly discussed in the paper.
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http://dx.doi.org/10.1016/j.watres.2016.12.001DOI Listing
March 2017

Emission characteristics of volatile compounds during sludges drying process.

J Hazard Mater 2009 Feb 13;162(1):186-92. Epub 2008 May 13.

Institute for Thermal Power Engineering, Zhejiang University, Hangzhou 310027, People's Republic of China.

The emission characteristics of volatile compounds (VCs) during municipal sewage sludge (MSS) and paper mill sludge (PMS) drying process were investigated through experiments conducted on a lab-scale tubular drying furnace and a pilot-scale paddle dryer, respectively. The result indicated that five kinds of VCs, i.e. CO(2), NH(3), C(7)H(16) (n-heptane), volatile fatty acids (VFAs) and CH(4) were emitted during the drying process. It was found that the NH(3) and CO(2) were the primary compound released from the MSS drying process. In the case of the PMS, the VFAs and CO(2) were the main compounds released. The temperature and water content of sludge had great effects on the emission rates of NH(3), C(7)H(16), CO(2) and VFAs. The pH and chemical oxygen demand (COD) of condensate from the paddle dryer were also studied. It showed that pH and COD of condensate from MSS were much higher than that from the PMS, and that the higher COD value of the MSS condensate interrelated to the higher ammonium and sulfur content of it.
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http://dx.doi.org/10.1016/j.jhazmat.2008.05.022DOI Listing
February 2009

Neuroprotection of lamotrigine on hypoxic-ischemic brain damage in neonatal rats: Relations to administration time and doses.

Biologics 2008 Jun;2(2):339-44

Department of Neurology, Institute of Neurosciences and the Second Affiliated Hospital.

Lamotrigine (LTG), an antiepileptic drug, has been shown to be able to improve cerebral ischemic damage by limiting the presynaptic release of glutamate. The present study investigated further the neuroprotective effect of LTG on hypoxic-ischemic brain damage (HIBD) in neonatal rats and its relations to administration time and doses. The HIBD model was produced in 7-days old SD rats by left common carotid artery ligation followed by 2 h hypoxic exposure (8% oxygen). LTG was administered intraperitoneally with the doses of 5, 10, 20, and 40 mg/kg 3 h after operation and the dose of 20 mg/kg 1 h before and 3 h, 6 h after operation. Blood and brain were sampled 24 h after operation. Nissl staining, terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL), and neuron-specific enolase (NSE) immunohistochemical staining were used for morphological studies. Water content in left cortex and NSE concentration in serum were determined. LTG significantly reduced water content in the cerebral cortex, as well as the number of TUNEL staining neurons in the dentate gyrus and cortex in hypoxic-ischemia (HI) model. Furthermore, LTG significantly decreased the NSE level in serum and increased the number of NSE staining neurons in the cortex. These effects, except that on water content, were dose-dependent and were more remarkable in the pre-treated group than in the post-treated groups. These results demonstrate that LTG may have a neuroprotective effect on acute HIBD in neonates. The effect is more prominent when administrated with higher doses and before HI.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2721363PMC
http://dx.doi.org/10.2147/btt.s2752DOI Listing
June 2008