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Sun H.-J.,Nanjing University | Rathinasabapathi B.,University of Florida | Wu B.,Nanjing University | Luo J.,Nanjing University | And 3 more authors.
Environment International | Year: 2014

Arsenic (As) and selenium (Se) are unusual metalloids as they both induce and cure cancer. They both cause carcinogenesis, pathology, cytotoxicity, and genotoxicity in humans, with reactive oxygen species playing an important role. While As induces adverse effects by decreasing DNA methylation and affecting protein 53 expression, Se induces adverse effects by modifying thioredoxin reductase. However, they can react with glutathione and S-adenosylmethionine by forming an As-Se complex, which can be secreted extracellularly. We hypothesize that there are two types of interactions between As and Se. At low concentration, Se can decrease As toxicity via excretion of As-Se compound [(GS3)2AsSe]-, but at high concentration, excessive Se can enhance As toxicity by reacting with S-adenosylmethionine and glutathione, and modifying the structure and activity of arsenite methyltransferase. This review is to summarize their toxicity mechanisms and the interaction between As and Se toxicity, and to provide suggestions for future investigations. © 2014.


Chavalitdhamrong D.,University of Florida | Donepudi S.,University of Florida | Pu L.,University of Florida | Pu L.,Suzhou Health College | Draganov P.V.,University of Florida
Digestive Endoscopy | Year: 2014

Endoscopic retrograde cholangiopancreatography (ERCP) has become a primary tool for the treatment of biliary and pancreatic ductal diseases. It is essential for the endoscopist carrying out the ERCP to have a thorough understanding of the potential adverse events. Typically, endoscopists are well familiar with common adverse events such as post-ERCP pancreatitis, cholangitis, post-sphincterotomy bleeding, post-sphincterotomy perforation, and sedation-related cardiopulmonary compromises. However, there are other less common adverse events that arecritical to promptly recognize in order to provide appropriate therapy and prevent disastrous outcomes. This review focuses on the presentation and management of the less common and rare adverse events of an ERCP from the perspective of the practicing endoscopist. © 2013 The Authors. Digestive Endoscopy © 2013 Japan Gastroenterological Endoscopy Society.


Xiang M.,Biotechnology Center | Wang J.,Suzhou Health College | Zhang Y.,Biotechnology Center | Ling J.,Suzhou Health College | Xu X.,Henan Provincial Institute of Food and Drug Control
Archives of Pharmacal Research | Year: 2012

Vascular complications are the leading causes of morbidity and mortality in diabetes mellitus (DM). The RAGE (receptor for advanced glycation end products)-NADPH oxidase-NF-κB signal transduction pathway plays an important role in the development of oxidative stressrelated vascular complications in DM. Ursolic acid (UA), a pentacyclic triterpenoid derived from plants, has been reported to have multiple pharmacological effects, including a potent antioxidant activity. This study aimed to investigate both the effect of UA on aortic injury in streptozotocin (STZ)-induced diabetic rats and the drug's mechanism of action. STZ-induced diabetic animals were randomized in one of the following 4 groups: no treatment (diabetic model group), aminoguanidine (AG, 100 mg/kg), high-dose UA (50 mg/kg), and low-dose UA (25 mg/kg). A non-diabetic control group was followed concurrently. After 8 weeks, the diabetic model rats exhibited: severe aortic arch injury, histologically elevated serum glucose, fructosamine, and glycosylated hemoglobin; and accumulation of advanced glycation end products (AGEs) in the arota. In addition, the levels of RAGE protein, transcription factor NF-κB p65, and the p22phox subunit of NADPH oxidase were increased, as were the serum levels of malondialdehyde and tumor necrosis factor-alpha (TNF-α; p < 0.01 vs control), suggesting that the mechanisms of oxidative stress contributed to vascular injury in the diabetic model group. In contrast, rats treated with UA (50 mg/kg) had a markedly less vascular injury and significantly improved biochemical parameters. Oxidative balance was also normalized in the UAtreated rats, and a marked reduction in the levels of RAGE and p22phox paralleled the reduced activation of NF-κB p65 and TNF-α (p < 0.01 and p < 0.05, respectively, vs diabetic model). These findings suggest that UA may suppress oxidative stress, thus blunting activation of the RAGE-NADPH oxidase-NF-κB signal transduction pathway, to ameliorate vascular injury in the STZ-induced DM rats.


Shen L.,Soochow University of China | Liu Z.,Suzhou Health College | Tu Y.,Soochow University of China | Xu L.,Soochow University of China | And 2 more authors.
Molecular Biology Reports | Year: 2011

β-1,3-N-acetylglucosaminyltransferase-8(β3Gn-T8) catalyzes the transfer of GlcNAc to the non-reducing terminus of the Galβ1-4GlcNAc of tetraantennary N-glycan in vitro. It has been reported to be involved in malignant tumors, but a comprehensive understanding of how the glycolsyltransferase correlates with the invasive potential of human gastric cancer is not currently available. Therefore, we investigated the ability and possible mechanism involved with β3Gn-T8 in modulating matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-2 (TIMP-2) in AGS gastric cancer cells. Here, we found out that siRNA-mediated suppression of the β3Gn-T8 could directly reduce the MMP-2 expression and activity as observed in RT-PCR, western blot and gelatin zymography analysis. Meanwhile, TIMP-2 expression had been increased. Cell invasion assay using matrigel matrix-coated transwell inserts showed that the invasive property was greatly suppressed in β3Gn-T8 siRNA transfected cells. Furthermore, cells overexpressing β3Gn-T8 gene (when transfected with pEGFP-C1 plasmid) also expressed MMP-2 gene, but TIMP-2 expression had been inhibited. The invasive ability of these cells was also enhanced. Protein-protein interaction analysis using STRING database showed that β3Gn-T8 and MMP-2 may have related signal pathway. In summary, our results reveal a new mechanism by which β3Gn-T8 can regulate MMP-2 and TIMP-2. We suggest that β3Gn-T8 can be used as a novel therapeutic target for human gastric treatment. © 2010 Springer Science+Business Media B.V.


Nicolae C.M.,Pennsylvania State University | Aho E.R.,Pennsylvania State University | Aho E.R.,Vanderbilt University | Choe K.N.,Pennsylvania State University | And 6 more authors.
Nucleic Acids Research | Year: 2015

Genomic instability, a major hallmark of cancer cells, is caused by incorrect or ineffective DNA repair. Many DNA repair mechanisms cooperate in cells to fight DNA damage, and are generally regulated by post-translational modification of key factors. Poly-ADP-ribosylation, catalyzed by PARP1, is a posttranslational modification playing a prominent role in DNA repair, but much less is known about mono- ADP-ribosylation. Here we report that mono-ADPribosylation plays an important role in homologous recombination DNA repair, a mechanism essential for replication fork stability and double strand break repair. We show that the mono-ADP-ribosyltransferase PARP14 interacts with the DNA replication machinery component PCNA and promotes replication of DNA lesions and common fragile sites. PARP14 depletion results in reduced homologous recombination, persistent RAD51 foci, hypersensitivity to DNA damaging agents and accumulation of DNA strand breaks. Our work uncovered PARP14 as a novel factor required for mitigating replication stress and promoting genomic stability. © The Author(s) 2015. Published by Oxford University Press on behalf of Nucleic Acids Research.


Liu Q.,Soochow University of China | Chen W.,Soochow University of China | Jiao Y.,Soochow University of China | Hou J.,Soochow University of China | And 4 more authors.
Journal of Surgical Research | Year: 2014

Background Many natural compounds possess antitumor growth activities. Pulsatilla chinensis is an herb used in traditional Chinese medicine to treat infectious diseases. More recently, extracts from P chinensis have been shown to contain antitumor activities. Materials and methods In this study, we isolated Pulsatilla saponin A as an active compound from P chinensis extracts and tested its anticancer activity in vitro and in vivo. Results In cell culture, Pulsatilla saponin A significantly inhibited the growth of human hepatocellular carcinoma SMCC-7721 cells and pancreatic BXPC3 and SW1990 cancer cells. Similar inhibitory activities were observed when the compound was tested in mouse xenograft tumor models using human hepatocellular carcinoma Bel-7402 and pancreatic cancer SW1990 cells. In Comet assay and flow cytometric analysis of cell cycle distribution and annexin V expression, DNA damage, G2 arrest, and apoptosis were identified in Pulsatilla saponin A-treated cancer cells. Based on the results of Western blotting, p53 and cyclin B protein levels were higher, whereas Bcl-2 protein levels were lower in Pulsatilla saponin A-treated cancer cells than in vehicle-treated cells. Conclusions Pulsatilla saponin A may exert its antitumor effect by inducing DNA damage and causing G2 arrest and apoptosis in cancer cells. Pulsatilla saponin A and its derivatives may be developed as a new class of anticancer agents. © 2014 Elsevier Inc. All rights reserved.


Yi L.X.,Suzhou Health College
Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology | Year: 2012

To explore the mechanisms by which splicing factor SC35 regulates the costimulatory molecule B7-H3 expression in vitro through bioinformatic and molecular biological methods. We screened some regulatory proteins which might take part in regulating B7-H3 expression using bioinformatic methods. Then RNA interference (RNAi) and real-time PCR were performed to test if these proteins took part in the regulation. Splicing factor SC35, SRP40 and SF50 might play an important role in the regulation of B7-H3 expression. In PHA-activated T cells, B7-H3 was upregulated obviously and at the same time SC35 was also upregulated. When we suppressed SC35 expression using RNAi, we found B7-H3 was also downregulated. Splicing factor SC35 might take part in the regulation of B7-H3 expression, which could help understand B7-H3 biological function.


Lei J.,Suzhou Health College | Ye K.,Suzhou Municipal Hospital | Zhu T.-M.,Suzhou Health College
International Journal of Clinical and Experimental Medicine | Year: 2016

Purpose: Inflammation is reported to play an important part in mediating injury in neonatal hypoxic-ischemic encephalopathy (HIE). Whether inflammatory-related cytokine such as IL-6 and TNF-α is associated with risk of HIE remains unknown. Method: In this meta-analysis of 29 clinical trials published to date in Chinese VIP, Wangfang, CNKI, Pubmed, Google Scholar database using the keywords “IL-6”, “TNF-α” and “hypoxic-ischemic encephalopathy/HIE”, we selected eligible studies which met the inclusion criterion, extract interested information and analyzed outcomes using the Review Manage 5.3 software. Results: Meta-analysis including 1618 HIE newborns and 790 healthy controls showed that serum IL-6 was significant up-regulated in different states (mild, moderate, severe) of neonatal hypoxic-ischemic encephalopathy (HIE) with the value of IV was 2.62, 4.91, 6.55, 95% CI [2.03, 3.22], [4.01, 5.80], [5.46, 7.64] and P<0.01. Similarly, compared to healthy controls, elevated serum TNF-α was also found to be associated with risk of neonatal HIE, the value of Std. Mean. Difference was 4.00, 4.75, 8.24, 95% CI was [3.60, 4.40], [4.07, 5.43], [7.38, 9.11] and P value <0.01. Conclusion: Meta-analysis suggested that elevated serum IL-6 and TNF-α level in newborns is associated with high risk of hypoxic-ischemic encephalopathy (HIE)-induced brain injury. Further studies are needed to validate these observations. © 2016, E-Century Publishing Corporation. All Rights Reserved.


Ding M.,Suzhou Health College | Ding M.,Rush University Medical Center | Xu J.Y.,Nanjing Medical University | Fan Y.,Nanjing Medical University
Oral Diseases | Year: 2010

Objective: To explore a potential causal contribution of the transcription factor HIF-1α and its target gene, RTP801 and VEGF, to the development of oral lichen planus (OLP). Design relevant: Twenty-two adult OLP patients were enrolled in this study. All OLP diagnoses were verified by histopathological characteristics. Normal mucous specimens were collected from 12 controls after various oral surgeries. Material and method: RNA was isolated from OLP and control specimens. Microarray was performed using BiostarH-40s gene chip. Expression of HIF-1α, VEGF and RTP801 was evaluated using quantitative real-time polymerase chain reaction (qPCR). Unpaired t-test and one-way ANOVA was used for statistical analysis. Results: Microarray results showed that RTP801 expression was lower in OLP than in controls (779 vs 3090). qPCR further confirmed that expression of RTP801 was similarly lower in OLP than in controls (0.363 vs 1.473, P < 0.001); expression of VEGF was also lower in OLP (0.448 vs 1.74, P = 0.012). In contrast, expression of HIF-1α was higher in OLP than in controls (11.12 vs 1.628, P < 0.001). Conclusion: The oral mucosa of OLP is hypoxic. Genes that are activated by hypoxia, such as RTP801 and VEGF, and their signal cascades may be novel potential therapeutic targets for OLP. © 2010 John Wiley & Sons A/S.


PubMed | University of North Texas Health Science Center, Suzhou Health College and Shanghai University of Traditional Chinese Medicine
Type: Journal Article | Journal: BMC complementary and alternative medicine | Year: 2016

Homeostasis imbalance of intracellular Ca(2+) is one of the key pathophysiological factors in skeletal muscle injuries. Such imbalance can cause significant change in the metabolism of Ca(2+)-related biomarkers in skeletal muscle, such as superoxide dismutase (SOD), malondialdehyde (MDA) and creatine kinase (CK). Measurements of these biomarkers can be used to evaluate the degree of damage to human skeletal muscle cells (HSKMCs) injury. Rolling manipulation is the most popular myofascial release technique in Traditional Chinese Medicine. The mechanism of how this technique works in ameliorating muscle injury is unknown. This study aimed to investigate the possible Ca(2+) mediated effects of intermittent pressure imitating rolling manipulation (IPIRM) of Traditional Chinese Medicine in the injured HSKMCs.The normal HSKMCs was used as control normal group (CNG), while the injured HSKMCs were further divided into five different groups: control injured group (CIG), Rolling manipulation group (RMG), Rolling manipulation-Verapamil group (RMVG), static pressure group (SPG) and static pressure-Verapamil group (SPVG). RMG and RMVG cells were cyclically exposed to 9.5-12.5N/cm(2) of IPIRM at a frequency of 1.0Hz for 10min. SPG and SPVG were loaded to a continuous pressure of 12.5N/cm(2) for 10min. Verapamil, a calcium antagonist, was added into the culture mediums of both RMVG and SPVG groups to block the influx of calcium ion.Compared with the CNG (normal cells), SOD activity was remarkably decreased while both MDA content and CK activity were significantly increased in the CIG (injured cells). When the injured cells were treated with the intermittent rolling manipulation pressure (RMG), the SOD activity was significantly increased and MDA content and CK activity were remarkably decreased. These effects were suppressed by adding the calcium antagonist Verapamil into the culture medium in RMVG. On the other hand, exposure to static pressure in SPG and SPVG affected neither the SOD activity nor the MDA content and CK activity in the injured muscle cells regardless of the presence of verapamil or not in the culture medium.These data suggest that the intermittent rolling pressure with the manipulation could ameliorate HSKMCs injury through a Ca(2+) dependent pathway. Static pressure did not lead to the same results.

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