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Publications (14)58.58 Total impact

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    ABSTRACT: Type 2 diabetes is a chronic inflammatory disease. A number of studies have clearly demonstrated that cytokines such as interleukin 1β (IL1β) contribute to pancreatic inflammation, leading to impaired glucose homeostasis and diabetic disease. There are findings which suggest that islet β-cells can secrete cytokines and cause inflammatory responses. In this process, thioredoxin-interacting protein (TXNIP) is induced by endoplasmic reticulum (ER) stress, which further demonstrates a potential role for ER stress in innate immunity via activation of the NOD-like receptor (NLRP) 3/caspase1 inflammasome and in diabetes pathogenesis via the release of cytokines. Recent developments have also revealed a crucial role for the autophagy pathway during ER stress and inflammation. Autophagy is an intracellular catabolic system that not only plays a crucial role in maintaining the normal islet architecture and intracellular insulin content but also represents a form of programmed cell death. In this review, we focus on the roles of autophagy, inflammation, and ER stress in type 2 diabetes but, above all, on the connections among these factors.
    General and Comparative Endocrinology 09/2014; · 2.82 Impact Factor
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    ABSTRACT: Thyroid cancers with unsatisfactory curative effect nowadays are the most common malignant tumors of the endocrine system. Apoptosis evasion, a hallmark of cancer, has driven the search of stimulating novel cell death way in cancer therapy. This review aims to explore the relationship between autophagy and thyroid cancer, especially the chemotherapy agents which are based on autophagy in treating thyroid cancers. A computerized literature search of MEDLINE was performed using the following search terms: autophagy and thyroid cancer. Recent studies have found that several chemotherapeutic agents and knockdown of specific microRNA may contribute to autophagic tumor cell death in most thyroid cancer types. Stimulating autophagy may be an effective alternative treatment to most types of thyroid cancer.
    Cancer Chemotherapy and Pharmacology 12/2013; · 2.80 Impact Factor
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    ABSTRACT: BACKGROUND: The pathophysiology of type 2 diabetes is progressive pancreatic beta cell failure with consequential reduced insulin secretion. Glucotoxicity results in the reduction of beta cell mass in type 2 diabetes by inducing apoptosis. Autophagy is essential for the maintenance of normal islet architecture and plays a crucial role in maintaining the intracellular insulin content by accelerating the insulin degradation rate in beta cells. Recently more attention has been paid to the effect of autophagy in type 2 diabetes. The regulatory pathway of autophagy in controlling pancreatic beta cells is still not clear. The aim of our study was to evaluate whether liraglutide can inhibit apoptosis and modulate autophagy in vitro in insulinoma cells (INS-1 cells). METHODS: INS-1 cells were incubated for 24 hours in the presence or absence of high levels of glucose, liraglutide (a long-acting human glucagon-like peptide-1 analogue), or 3-methyadenine (3-MA). Cell viability was measured using the Cell Counting Kit-8 (CCK8) viability assay. Autophagy of INS-1 cells was tested by monodansylcadaverine (MDC) staining, an autophagy fluorescent compound used for the labeling of autophagic vacuoles, and by Western blotting of microtubule-associated protein I light chain 3 (LC3), a biochemical markers of autophagic initiation. RESULTS: The viability of INS-1 cells was reduced after treatment with high levels of glucose. The viability of INS-1 cells was reduced and apoptosis was increased when autophagy was inhibited. The viability of INS-1 cells was significantly increased by adding liraglutide to supplement high glucose level medium compared with the cells treated with high glucose levels alone. CONCLUSIONS: Apoptosis and autophagy were increased in rat INS-1 cells when treated with high level of glucose, and the viability of INS-1 cells was significantly reduced by inhibiting autophagy. Liraglutide protected INS-1 cells from high glucose level-induced apoptosis that is accompanied by a significant increase of autophagy, suggesting that liraglutide plays a role in beta cell apoptosis by targeting autophagy. Thus, autophagy may be a new target for the prevention or treatment of diabetes.
    Chinese medical journal 03/2013; 126(5):937-941. · 0.90 Impact Factor
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    ABSTRACT: T1D (type 1 diabetes) is an autoimmune disease characterized by lymphocytic infiltration, or inflammation in pancreatic islets called 'insulitis.' Comparatively speaking, T2D (type 2 diabetes) is traditionally characterized by insulin resistance and islet β cell dysfunction; however, a number of studies have clearly demonstrated that chronic tissue inflammation is a key contributing factor to T2D. The NLR (Nod-like receptor) family of innate immune cell sensors such as the NLRP3 inflammasome are implicated in leading to CASP1 activation and subsequent IL1B (interleukin 1, β) and IL18 secretion in T2D. Recent developments reveal a crucial role for the autophagy pathway under conditions of oxidative stress and inflammation. Increasingly, research on autophagy has begun to focus on its role in interacting with inflammatory processes, and thereby how it potentially affects the outcome of disease progression. In this review, we explore the pathophysiological pathways associated with oxidative stress and inflammation in T2D. We also explore how autophagy influences glucose homeostasis by modulating the inflammatory response. We will provide here a perspective on the current research between autophagy, inflammation and T2D.
    Autophagy 01/2013; 9(3). · 12.04 Impact Factor
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    ABSTRACT: Hyperglycemia is the major cause of diabetic angiopathy. Sarpogrelate hydrochloride is an antiplatelet drug, and expected to be useful in the treatment of chronic arterial occlusive diseases. The aim of our study was to evaluate the possible effects of sarpogrelate hydrochloride on adhesion molecule expression and its underlying mechanism in the prevention and treatment of cardiovascular disorders. Intercellular adhesion molecule-1 (ICAM-1) expression and superoxide dismutase (SOD) activity were determined after endothelial cells were exposed to high glucose in the absence and presence of sarpogrelate hydrochloride. Coincubation of endothelial cells with high glucose for 24 h resulted in a significant increase of monocyte-endothelial cell adhesion and the expression of ICAM-1 (P < 0.01). These effects were abolished by sarpogrelate hydrochloride and sarpogrelate hydrochloride significantly increased SOD activities (40 ± 8 vs. 47 ± 7, n = 8, P < 0.01). The low dose sarpogrelate group (0.1 μM) had significantly higher monocyte-endothelial cell adhesion and the expression of ICAM-1 than medium dose sarpogrelate group (1.0 μM) and high dose sarpogrelate group (10.0 μM) (P < 0.05 for comparison among three groups and P < 0.01 for difference between low and high dose sarpogrelate groups). These findings suggested that sarpogrelate hydrochloride was able to protect vascular endothelium from dysfunction induced by high glucose.
    Molecular and Cellular Biochemistry 10/2012; · 2.33 Impact Factor
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    ABSTRACT: OBJECTIVES: The aims of this study were to examine the effects of KB-R7943, an inhibitor of Na(+)/Ca(2+) exchanger, on impaired endothelium-dependent relaxation (EDR) induced by advanced glycosylation end products (AGE) in isolated rat aorta. METHODS: Both acetylcholine (ACh)-induced EDR and sodium nitroprusside (SNP)-induced endothelium-independent relaxation (EIR) were measured after the rings were exposed to AGE in the absence and presence of KB-R7943. RESULTS: Co-incubation of aortic rings with AGE (0.1g/L) for 24h resulted in a significant inhibition of EDR, but had no effects on EIR. After incubation of the rings in the co-presence of KB-R7943 (0.1-10μM) with AGE for 24h, KB-R7943 (10μM) significantly attenuated impaired EDR. Superoxide dismutase (200 U/mL) and l-arginine (3mM) could ameliorate the impairment of EDR caused by AGE, whereas d-arginine (3mM) had no effect on EDR. Similarly, AGE decreased superoxide dismutase (SOD) activity and the release of nitric oxide (NO), and increased superoxide anion (O(2)(.-)) production in aortic tissue. KB-R7943 (10μM) significantly decreased O(2)(.-) production and increased SOD activity and the NO release. CONCLUSIONS: These results suggest that KB-R7943 attenuated the impairment of EDR elicited by AGE partially through scavenging oxygen free radicals.
    Journal of diabetes and its complications 09/2012; · 2.11 Impact Factor
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    ABSTRACT: Cardiovascular complications account for significant morbidity and mortality in the diabetic population. Diabetic cardiomyopathy (DCM), a prominent cardiovascular complication, has been recognized as a microvascular disease that may lead to heart failure. During the past few decades, research progress has been made in investigating the pathophysiology of the disease; however, the exact molecular mechanism has not been elucidated, making therapeutic a difficult task. In this review article, we have discussed a number of diabetes-induced metabolites such as glucose, advanced glycation end products, protein kinase C, free fatty acid and oxidative stress and other related factors that are implicated in the pathophysiology of the DCM. An understanding of the biochemical and molecular changes especially early in the DCM may lead to new and effective therapies toward prevention and amelioration of DCM, which is important for the millions of individuals who already have or are likely to develop the disease before a cure becomes available.
    Biochemical and Biophysical Research Communications 09/2012; 427(3):441-3. · 2.28 Impact Factor
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    ABSTRACT: Diabetes mellitus (DM) is a serious metabolic disorder with micro- and macrovascular complications that results in significant morbidity and mortality. It is well established that cytosolic Ca(2+) play an important role in controlling insulin secretion in pancreatic β-cells. The Na(+)/Ca(2+) exchanger (NCX), an ion transport protein, is expressed in the plasma membrane of virtually all animal cells. NCX is a reversible carrier that can mediate the transport of Ca(2+) across the plasma membrane in both directions. Therefore, great efforts have been made to identify NCX associated with DM. NCX is expressed in several tissues, and acts in the protection against intracellular calcium overload; in the regulation of insulin secretion by beta cells, and in improving vascular endothelium-dependent relaxation. All these mechanisms are associated with DM pathogenesis and its chronic complications. Therefore, NCX is a candidate protein for the development of these disorders. Only a few studies investigated NCX in relation to chronic complications of diabetes, with inconclusive results.
    Biochemical and Biophysical Research Communications 09/2012; 426(4):445-7. · 2.28 Impact Factor
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    ABSTRACT: In pancreatic β-cells, the endoplasmic reticulum (ER) is the crucial site for insulin biosynthesis, as this is where the protein-folding machinery for secretory proteins is localized. Perturbations to ER function of the β-cell, such as those caused by high levels of free fatty acid and insulin resistance, can lead to an imbalance in protein homeostasis and ER stress, which has been recognized as an important mechanism for type 2 diabetes. Macroautophagy (hereafter referred to as autophagy) is activated as a novel signaling pathway in response to ER stress. In this review, we outline the mechanism of ER stress-mediated β-cell death and focus on the role of autophagy in ameliorating ER stress. The development of drugs to take advantage of the potential protective effect of autophagy in ER stress, such as glucagon like peptide-1, will be a promising avenue of investigation.
    Autophagy 02/2012; 8(2):158-64. · 12.04 Impact Factor
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    ABSTRACT: Diabetic nephropathy is characterized by the accumulation of extracellular matrix in the glomerular mesangium as a result of an imbalance between matrix synthesis and degradation. Since simvastatin has been proposed to decrease renal interstitial fibrosis, we hypothesized that the protective effect of statins was related to the expression of transforming growth factor-β (TGF-β) and type IV collagen (Col IV). Cultured rat mesangial cells (RMC) were exposed to high glucose (HG), advanced glycosylation end products (AGE) or H(2)O(2) in the absence and presence of simvastatin. Expression of TGF-β and Col IV was determined by Western blotting. Coincubation of RMC with HG, AGE or H(2)O(2) resulted in a significant increase of the expression of TGF-β and Col IV (p < 0.05). Simvastatin significantly inhibited HG-, AGE- or H(2)O(2)-induced expression of TGF-β and Col IV (p < 0.05). Moreover, simvastatin also inhibited HG-, AGE- and H(2)O(2)-induced activation of p38 mitogen-activated protein kinase, which indicated that the preventive effect of simvastatin on TGF-β and Col IV may be associated with p38. These findings suggest that simvastatin can reduce HG-, AGE- and H(2)O(2)-induced expression of TGF-β and Col IV by inhibition of the p38 pathway.
    Pharmacology 09/2011; 88(3-4):188-92. · 1.60 Impact Factor
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    ABSTRACT: Autophagy is an intracellular catabolic system, which enables cells to capture cytoplasmic components for degradation within lysosomes. Autophagy is involved in development, differentiation and tissue remodeling in various organisms, and is also implicated in certain diseases. Recent studies demonstrate that autophagy is necessary to maintain architecture and function of pancreatic beta cells. Altered autophagy is also involved in pancreatic beta cell death. Whether autophagy plays a protective or harmful role in diabetes is still not clear. In this review, we will summarize the current knowledge about the role of autophagy in pancreatic beta cell and diabetes.
    Autophagy 01/2011; 7(1):12-6. · 12.04 Impact Factor
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    ABSTRACT: Selenium as a component of glutathione peroxidase may be beneficial in insulin resistance, hence potentially may modify the risk of diabetes and cardiovascular disease. The aim of our study was to evaluate whether selenium can also alter high glucose (HG), advanced glycation end products (AGE), high insulin (HI) and H2O2-induced expression of cyclooxygenase (COX)-2 and P-selectin. Human umbilical vein endothelial cells (HUVECs) were pretreated with selenium and stimulated by HG, AGE, HI and H2O2. Selenium significantly inhibited HG, AGE, HI and H2O2-induced expression of COX-2 and P-selectin. Moreover, selenium also inhibited HG, AGE, HI and H2O2-induced activation of p38 mitogen-activated protein kinase (p38 MAPK), which indicated that the preventive effects of selenium on COX-2 and P-selectin may be associated with p38. Our results indicated that selenium supplementation can reduce HG, AGE, HI and H2O2-induced expression of COX-2 and P-selectin by inhibition of the p38 pathway.
    Molecular Biology Reports 11/2010; 38(4):2301-6. · 2.51 Impact Factor
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    ABSTRACT: The aim of this study was to determine the effects of simvastatin and atorvastatin on the markers of oxidative stress in patients with type 2 diabetes mellitus (T2DM). The study population consisted of 151 patients with T2DM and 147 control individuals. The patients with T2DM were treated with 40 mg of simvastatin per day or 10 mg of simvastatin per day. Waist circumference, body mass index, blood pressure, and glucose and insulin values were obtained; and fasting serum lipids, malondialdehyde, nitric oxide, glutathione peroxidase and superoxide dismutase activity were determined before and after 12 weeks of treatment. Statin treatment significantly decreased plasma lipids in all patients with diabetes (P < 0.05). No significant differences were detected between the two treatment groups with respect to plasma lipid profile (P < 0.05). In addition, the effects of atorvastatin to increase nitric oxide concentration (33.28 +/- 3.37 micromol/L versus 27.32 +/- 4.15 micromol/L, P < 0.05) and glutathione peroxidase (17.67 +/- 1.41 micromol/L versus 14.28 +/- 1.65 micromol/L, P < 0.05), superoxide dismutase activity (34.28 +/- 4.71 micromol/L versus 27.91 +/- 3.38 micromol/L, P < 0.05 ) and decreased malondialdehyde level (49.52 +/- 5.67 micromol/L versus 42.08 +/- 5.16 micromol/L, P < 0.05) were significantly greater in patients with T2DM compared with simvastatin. The changes in the markers of oxidative stress did not correlate with the changes in plasma lipid profile (P > 0.05). This study suggested that atorvastatin reduced oxidative stress more effectively than simvastatin in patients with T2DM and the clinical benefits of statins may be independent of their cholesterol-lowering effects.
    Journal of cardiovascular pharmacology 09/2009; 55(1):21-5. · 2.83 Impact Factor
  • Yan-bo Li, Wei-min Li, Jun-yong Han
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    ABSTRACT: To study the relationship between P38MAPK and MCP-1 in diabetic HUVEC and the mechanism of anti-atherosclerosis of selenium. HUVEC were treated with high concentration of glucose, advanced glycosylation end products (AGE), high concentration of insulin or H(2)O(2) with or without pre-treatment with SB203580 (P38MAPK specific inhibitor) or selenium. The expression of phospho-P38MAPK and MCP-1 in HUVEC was detected by Western blot or RT-PCR, respectively. High concentration of glucose, AGE, high concentration of insulin and H(2)O(2) can activate P38MAPK and increase the expression of MCP-1 in HUVEC. The expression of MCP-1 was inhibited by SB203580. Selenium inhibited the activation of P38MAPK and reduced the expression of MCP-1. P38MAPK is an upstream signaling molecule of MCP-1. P38MAPK may be one of the initiating signals of diabetic atherosclerosis. Selenium can inhibit the expression of MCP-1 by repressing P38MAPK signaling pathway and therefore prevent the development of atherosclerosis.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 10/2005; 21(5):615-8.