Wuxi Higher Health Vocational Technology School

Wuxi, China

Wuxi Higher Health Vocational Technology School

Wuxi, China
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Qian J.,Shanghai University | Zhang J.-M.,Shanghai University | Lin L.-L.,Wuxi Higher Health Vocational Technology School | Dong W.-Z.,Shanghai University | And 3 more authors.
International Journal of Stroke | Year: 2015

Background: Increasing endogenous acetylcholine by neostigmine decreased the ischemic cerebral injury. The off-target action on muscarinic receptor produced a variety of adverse effects and limited the clinical application on stroke. Aim: We combined neostigmine with anisodamine and investigated the neuroprotection and mechanism. Methods: Male Sprague-Dawley rats were subjected to middle cerebral artery occlusion. Neuroprotective action of neostigmine in combination with anisodamine at varying ratios was examined to determine the optimal combination as well as ideal therapeutic window. Potential involvement of α7 nicotinic acetylcholine receptor was examined by measuring the infarct size, the expression of proinflammatory cytokines, and the biomarkers of apoptosis in α7 nicotinic acetylcholine receptor knockout mice. A set of in vitro experiments was conducted in RAW264.7 cells to probe into potential molecular mechanisms. Results: The neostigmine/anisodamine combination conferred neuroprotection. The protection was most potent at a ratio of 1:500. At such a ratio, the combination increased the binding of acetylcholine to α7 nicotinic acetylcholine receptor and reduced proinflammatory cytokines. The neuroprotection was evident only in wild-type and not in α7 nicotinic acetylcholine receptor knockout mice. The combination significantly decreased the expression of Bad and Bax, and increased Bcl-2 and Bcl-xl in α7 nicotinic acetylcholine receptor wild-type mice but not in knockout mice. The combination did not affect caspase-8, cleaved caspase-8, or caspase-12. Conclusions: Current study identified the optimal combination of neostigmine and anisodamine against ischemic stroke, and indicated that the acetylcholine-α7 nicotinic acetylcholine receptor is involved in the protective effects. © 2015 World Stroke Organization.

Wang W.,Shanghai University | Lin L.-L.,Shanghai University | Lin L.-L.,Wuxi Higher Health Vocational Technology School | Guo J.-M.,Shanghai University | And 7 more authors.
International Journal of Stroke | Year: 2015

Background: Heavy ethanol consumption is widely accepted as a risk for ischemic stroke. The molecular mechanisms of ethanol-induced brain injury have not been fully understood.Aim: This study aims to find out the mechanism of the ischemic cerebral injury.Methods: We used Sprague-Dawley rats with transient middle cerebral artery occlusion for acute experiment and stroke-prone spontaneously hypertensive rats for long-term experiment in vivo, and oxygen-glucose deprivation model in vitro to define a detrimental effect of different doses of ethanol on ischemic stroke injury. We also used mitochondrial aldehyde dehydrogenase 2 knockdown/overexpression or inhibitor/activator to investigate mechanism of the adverse effects of ethanol.Results: High-dose ethanol (36% of calorie derived from ethanol) significantly increased the infarct size in rats (P < 0·01) and decreased the survival time of stroke-prone spontaneously hypertensive rats by about 20%. Six-week treatment with high-dose ethanol changed a distribution of isoelectric point of aldehyde dehydrogenase 2 and inhibited aldehyde dehydrogenase 2 activity in brain. High dose of ethanol increased the cerebral acetaldehyde level, and increased 4-hydroxy-2-nonenal and malondialdehyde in serum of rats with middle cerebral artery occlusion. The activator of aldehyde dehydrogenase 2, Alda-1 abolished neuronal cells death and ischemic injury induced by ethanol and the inhibitor reversed the injurious effects. An overexpression of aldehyde dehydrogenase 2 completely abolished the increased infarct size and neurological deficit score by ethanol. Conversely, knockdown of aldehyde dehydrogenase 2 increased the infarct size and exaggerated the cerebral injury induced by ethanol.Conclusions: High concentrations of ethanol aggravate cerebral injury by inhibiting of aldehyde dehydrogenase 2 and inducing excess accumulation of aldehydes. © 2015 World Stroke Organization.

Hua B.-Y.,Wuxi Institute of Technology | Hua M.-J.,Wuxi Higher Health Vocational Technology School
Journal of Chemical and Pharmaceutical Research | Year: 2014

The sports injury is difficult to avoid for the basketball player, therefore the proper pharmaceutical treatment should be found out to deal with it. Firstly, the main pharmaceutical treatment methods of sports injury are discussed. Secondly, the causes of sports injury for the basketball player are analyzed. Thirdly, the clinical effect analysis of pharmaceutical treatment on the sports injure of basketball player is carried out, results show that this kind of Chinese pharmaceutical treatment can get better treatment effect. © 2014, Journal of Chemical and Pharmaceutical Research. All rights reserved.

Liu Y.,Wuxi Higher Health Vocational Technology School | Xie K.-M.,Suzhou University | Yang G.-Q.,Suzhou University | Bai X.-M.,Suzhou University | And 5 more authors.
Cancer Chemotherapy and Pharmacology | Year: 2010

We have previously shown that the expression of glucosylceramide synthase (GCS) gene in drug-resistant K562/AO2 human leukemia cell was higher than that in drug-sensitive K562 cell, and the sensitivity to adriamycin of K562/AO2 cell was enhanced by inhibiting GCS. It is concluded that the overexpression of GCS gene is one of the reasons which lead to multidrug resistance (MDR) of leukemia cell. Meanwhile, we also found that higher expression of Bcl-2 gene and protein were exhibited in K562/AO2 cell compared with K562 cell. Basing on this, we hypothesized that the high expression of GCS gene which results in MDR of leukemia cell is correlated with Bcl-2 signal transduction. In order to validate the hypothesis, the inhibition of GCS gene in K562/AO2 cell was observed by using chemical suppressor PPMP and siRNA targeted at GCS, and applying RT-PCR and flow cytometry, the expression levels of apoptosis-related gene Bcl-2 and Bax were analyzed before and after inhibiting GCS gene in K562/AO2 cell. The results demonstrated that the gene and protein of Bcl-2 in K562/AO2 cell were both down-regulated significantly after GCS gene being inhibited; however, the Bax mRNA expression had no apparent change in different groups. This suggested that GCS gene may contributed to MDR of human leukemia cell K562/AO2 by Bcl-2 signal transduction. © Springer-Verlag 2009.

Wang Q.,Jiangnan University | Wang Q.,Wuxi Higher Health Vocational Technology School | Ji J.,Jiangnan University | Jiang D.,Jiangnan University | And 3 more authors.
Analytical Methods | Year: 2014

A novel electrochemical sensor for acrylamide (AM) detection based on molecularly imprinted polymer (MIP) membranes was constructed. p-Aminothiophenol (P-ATP) and AM were assembled on the surface of a gold nanoparticle (AuNP) modified glass carbon electrode (GCE) by the formation of Au-S bonds and hydrogen-bonding interactions, and polymer membranes were formed by electropolymerization in a polymer solution containing P-ATP, HAuCl4, tetrabutylammonium perchlorate (TBAP) and a dummy template molecule propanamide (PMA). A novel molecularly imprinted sensor (MIS) was obtained after the removal of PMA. Cyclic voltammetry (CV) and differential pulse voltammetry (DPV) measurements were used to monitor the electropolymerization process and its optimization, which was further characterized by scanning electron microscopy (SEM). The linear response range of the MIS was between 1 × 10 -12 and 1 × 10-7 mol L-1, with a detection limit of 0.5 × 10-12 mol L-1. This research provides a fast, sensitive and real-time method for the detection of AM in a real sample without complex pretreatment and with average recoveries higher than 95% and a relative standard deviation (RSD) lower than 3.73%. All the obtained results indicate that the MIS is an effective electrochemical technique to determine AM in real-time and in a complicated matrix. This journal is © the Partner Organisations 2014.

Fan Y.-F.,Nanjing Medical University | Wu Y.-M.,Nanjing Medical University | Wu Y.-M.,The Third Peoples Hospital of Wuxi | Liu H.,Nanjing Medical University | And 5 more authors.
Human Immunology | Year: 2014

Helicobacter pylori infection is a risk factor for gastric cancer. In addition, toll-like receptor 4 (TLR4) plays a fundamental role in pathogen recognition and activation of innate immunity. This study investigated the association of TLR4 polymorphisms with a risk of intestinal metaplasia (IM) and intraepithelial neoplasia (IN) in a Chinese Han population. This study analyzed TLR4 gene polymorphisms in 333 patients (IM, 193 cases; IN, 140 cases) and 312 atypia-free controls in a Chinese Han population using a Taqman allelic discrimination assay. The TLR4 single nucleotide polymorphisms +896A/G and +1196C/T were not associated with the risk of IM or IN. However, the single-locus analysis showed that the C allele of TLR4+2856T/C had significantly reduced risk of IM and IN [adjusted odds ratio (OR). = 0.42; 95%CI. = 0.29-0.62 and OR. = 0.62; 95%CI. = 0.41-0.93, respectively] compared with the wild-type homozygote (TT). The frequencies of TLR4+2856T/C TC and T carrier were significantly lower in patients with Sydney's slight IM and low grade IN (P<. 0.01 and P= 0.01, respectively), while the TC genotype showed a lower risk of moderate IM compared to healthy controls (P= 0.045). In addition, the data revealed that H. pylori infection, heavy alcohol consumption and high salt uptake were associated with a higher susceptibility for developing this neoplasm. TLR4 rs10759932 TC and C carriers were associated with a lower risk in developing precancerous lesions in the stomach in a Chinese Han population. © 2013 American Society for Histocompatibility and Immunogenetics.

Wu Y.,Nanjing Medical University | Wu Y.,Third Peoples Hospital of Wuxi | Fan Y.,Nanjing Medical University | Jiang Y.,Wuxi Higher Health Vocational Technology School | And 3 more authors.
Journal of Cancer Research and Therapeutics | Year: 2013

Purpose: To investigate the association between various risk factors and precancerous lesion of gastric cancer (PLGC) in patients from eastern China. Materials and Methods: 501 cases of PLGC and 523 cases of superficial gastritis were included. A comparative study of the relation between different risk factors and PGLC was performed. Results: Statistical differences were noted in a series of indexes including Helicobacter pylori (HP) infection, family history of esophageal cancer (EC), gastric cancer (GC) and chronic atrophic gastritis (CAG), a history of CAG, gastric polyps (GP) and gastric ulcer (GU), usage of non-steroids (e.g., aspirin), gastroesophageal reflux disease (GERD), consuming alcohol, eating food rich in nitroso compounds, irregular eating habits with no breakfast, ingestion of smoked meat, fried food and spicy food, anxiety and depression. The risk factors associated with PLGC ranked in an order of a history of CAG, GP, family history of GC, usage of non-steroids (e.g., aspirin), ingestion of spicy food frequently, HP infection, family history of EC, consuming alcohol, anxiety, a history of GU, GERD and family history of CAG. Conclusions: A history of CAG was most associated with PLGC in patients from eastern China, followed by a history of GP and family history of GC.

Yao W.,Wuxi Higher Health Vocational Technology School | Zou H.-J.,Wuxi Higher Health Vocational Technology School | Sun D.,Wuxi Higher Health Vocational Technology School | Ren S.-Q.,Nanjing Medical University
Brain Research | Year: 2013

Beta-amyloid peptide (Aβ) has a causal role in the pathophysiology of Alzheimer's disease (AD). Recent studies indicate that Aβ can disrupt excitatory glutamatergic synaptic function at synaptic level. However, the underlying mechanisms remain obscure. In this study, we recorded evoked and spontaneous EPSCs in hippocampal CA1 pyramidal neurons via whole-cell voltage-clamping methods and found that 1 μM Aβ can induce acute depression of basal glutamatergic synaptic transmission through both presynaptic and postsynaptic dysfunction. Moreover, we also found that Aβ-induced both presynaptic and postsynaptic dysfunction can be reversed by the inhibitor of protein phosphatase 2B (PP2B), FK506, whereas only postsynaptic disruption can be ameliorated by the inhibitor of PP1/PP2A, Okadaic acid (OA). These results indicate that PP1/PP2A and PP2B have overlapping but not identical functions in Aβ-induced acute depression of excitatory glutamatergic synaptic transmission of hippocampal CA1 pyramidal neurons. © 2013 Elsevier B.V.

Ni Y.,Hangzhou Normal University | He X.,Hangzhou Normal University | Yuan Z.,Wuxi Higher Health Vocational Technology School | Liu M.,Hangzhou Normal University | And 2 more authors.
Annals of Plastic Surgery | Year: 2015

Objective This study aimed to compare the graft survival rates of various ratios of fat particles to stromal vascular fraction (SVF) in rabbits. Methods Fifteen purebred white rabbits of the same brood were used. In the study, the grafts of equal weight (0.8 g) were mixtures of fat particles with various proportions of SVF (1/3, 1/4, 1/5, and 1/6) to form 4 treated groups (I, II, III, and IV), whereas merely fat particles formed 1 control group. They were randomly autoimplanted into subcutaneous pockets on both sides of the dorsal midlines of the rabbits. Animals were killed 3 months after surgery. The grafts were harvested and weighed. Comparisons were performed between the groups for survival rates. Results The treated group II (fat particle-to-SVF ratio was 3:1) revealed the greatest weight maintenance in all of the groups, showing the greatest survival rate [87.94% (1.30%), P < 0.01 or P < 0.05]. Conclusions It was suggested that the optimal fat particle-to-SVF ratio might be 3:1, with a low resorption rate. © 2015 Wolters Kluwer Health, Inc. All rights reserved.

Li J.,Wuxi Higher Health Vocational Technology School | Qiu D.-M.,Wuxi Higher Health Vocational Technology School | Chen S.-H.,Wuxi Higher Health Vocational Technology School | Cao S.-P.,Wuxi Higher Health Vocational Technology School | Xia X.-L.,Wuxi Higher Health Vocational Technology School
Asian Pacific Journal of Cancer Prevention | Year: 2014

Background: Coptisine, an isoquinoline alkaloid extracted from Coptidis rhizoma, has many biological activities such as antidiabetic, antimicrobial and antiviral actions. However, whether coptisine exerts anti-cancer metastasis effects remains unknown. Materials and Methods: Effects of coptisine on highly metastatic human breast cancer cell MDA-MB-231 proliferation were evaluated by trypan blue assay and on cell adhesion, migration and invasion by gelatin adhesion, wound-healing and matrigel invasion chamber assays, respectively. Expression of two matrix metalloproteinases (MMPs), MMP-9, MMP-2 and their specific inhibitors tissue inhibitor of metalloproteinase 1 (TIMP-1) and tissue inhibitor of metalloproteinase 2 (TIMP-2) were analyzed by RT-PCR. Results: Coptisine obviously inhibited adhesion to an ECM-coated substrate, wound healing migration, and invasion through the matrigel in MDA-MB-231 breast cancer cells. RT-PCR revealed that coptisine reduced the expression of the ECM degradation-associated gene MMP-9 at the mRNA level, and the expression of TIMP-1 was up-regulated in MDA-MB-231 cells, while the expression of MMP-2 and its specific inhibitor TIMP-2 was not affected. Conclusions: Taken together, our data showed that coptisine suppressed adhesion, migration and invasion of MDA-MB-231 breast cancer cells in vitro, the down-regulation of MMP-9 in combination with the increase of TIMP-1 possibly contributing to the anti-metastatic function. Coptisine might be a potential drug candidate for breast cancer therapy.

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