First Peoples Hospital of Hefei

Anhui, China

First Peoples Hospital of Hefei

Anhui, China
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Zhang L.-J.,First Peoples Hospital of Hefei | Hu W.,Anhui Medical University | Tang J.,Anhui Medical University | Wu F.-R.,Anhui Medical University | And 3 more authors.
Chinese Pharmacological Bulletin | Year: 2014

Aim To study the role of ASICla on the matrix turnover and MAPK expression of the rat articular chondrocytes with extracellular acidosis.Methods Articular chondrocytes were isolated from Sprague-Dawley rats, and their phenotype was determined by toluidine blue and immunocytochemical staining. The GAG content of cell culture supernatant was determined by dimethyl-methylene blue spectrophotometric assay, while Hyp content by chloramine T assay. ELISA assay was used to measure MMP-2, TIMP-2 content. Furthermore, the ERK1/2, p38 MAPK phosphorylation protein expression levels were tested by Western blot assay.Results ASICla contributed to the effect of GAG, Hyp and TIMP-2 levels reduction induced by extracellular acidification, while the effect of MMP-2 was weaker. Moreover, ASICla could increase the ERK1/2, p38 MAPK phosphorylation protein expression levels.Conclusion ASICla could regulate rat articular chondrocytes matrix turnover via ERK1/2 and p38 MAPK signaling pathway, and thereby inhibit the rat articular cartilage damage induced by acidosis.

Su Z.-F.,Anhui Medical University | Sun Z.-W.,Anhui Medical University | Zhang Y.,First Peoples Hospital of Hefei | Wang S.,First Peoples Hospital of Hefei | And 2 more authors.
Kaohsiung Journal of Medical Sciences | Year: 2016

The study aims to explore how microRNA-146a/b (miR-146a/b) regulates the function of endothelial progenitor cells (EPCs) in acute ischemic stroke in mice. Eighty male SPF C57BL/6J mice were evenly divided into the model-6 h, model-12 h, model-24 h (mice suffered from middle cerebral artery occlusion [MCAO] for 6 h, 12 h and model-24 h) and normal groups. EPCs were transfected and assigned into the control, MCAO, MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. The qRT-PCR was used to detect miR-146a/b expression in EPCs. Expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were detected using western blotting. Cell proliferation and migration of EPCs were testified using CCK-8 assay and scratch test, respectively. Angiogenesis ability of EPCs was observed under microscope. MiR-146a and miR-146b expressions were lower in the model groups than the normal group. There were up-regulated TRAF6 and IRAK1 expressions in the model-6 h, model-12 h and model-24 h groups compared with the normal group. And there were down-regulated TRAF6 and IRAK1 expressions in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups than in the MCAO group. Compared with the control group, the proliferation, migration and angiogenesis ability of EPCs were significantly lower in the MCAO group, but higher in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. Besides, the miR-146a/b group showed more enhancement than the MCAO-miR-146a and MCAO-miR-146b groups. MiR-146a/b could down-regulate the TRAF6 and IRAK1 expressions and promote proliferation, migration and angiogenesis ability of EPCs, which was important for recovery of patients with hyperacute ischemic stroke. © 2017.

PubMed | Ningbo Development Zone Center Hospital, Wenzhou University, Shanghai University, Chinese People's Liberation Army and 2 more.
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

Osteosarcoma (OS) is the most frequent type of primitive malignant bone tumor with a poor prognosis due to distant metastasis. Our previous studies have demonstrated that IRX2 is overexpressed and is important in cell proliferation and invasion. However, the molecular mechanisms underlying the IRX2dependent regulation of OS progression remains to be elucidated. In the present study, the effects of IRX2 on the upregulation of MMP2 and VEGF in OS were determined by western blotting, and the underlying molecular mechanisms were elucidated. These findings provided data suggesting that IRX2 modulates the expression levels of MMP2 and VEGF in an AKTdependent manner. The overexpression of IRX2 promoted the activation of PI3K/Akt and increased the proliferation and invasiveness of the OS cell lines as shown by CCK8 and invasion assays. Notably, interruption of the AKT pathway by treatment with LY294002, a specific PI3K inhibitor, attenuated IRX2induced cell proliferation and invasive ability, and the upregulation of MMP2 and VEGF. The results of the present study suggested that inhibition of the IRX2mediated AKT signaling pathway may be a suitable therapeutic target for the treatment of OS.

Li Y.,Nanjing University | Tian Y.,Nanjing Medical University | Zhu W.,Nanjing University | Gong J.,Nanjing University | And 5 more authors.
International Immunopharmacology | Year: 2013

Background IL-6/STAT3/SOCS3 signaling pathway plays an important role in the pathogenesis of Crohn's disease by induction of the antiapoptotic factors Bcl-2 and Bcl-xl in lamina propria mononuclear cells (LPMCs). We previously reported that triptolide showed therapeutic activity in mouse colitis by mechanisms involving suppression of IL-6 trans-signaling. IL-10 gene-deficient mice with established colitis were used for the experiments with triptolide administration. Methods This study further investigates the mechanism by which triptolide attenuates Crohn's colitis. IL-10 gene-deficient mice (IL-10 -/-) of 10-12 weeks with established colitis were used for the experiments with chronic triptolide administration. Apoptosis of lamina propria mononuclear cells (LPMCs) were measured by flow cytometry. SOCS, Bcl-2, Bcl-xl and Bax were determined by Western blot. Furthermore, an in vitro study was performed by using cultured intestine from CD patients to observe the direct effects of triptolide. Results Our data indicated triptolide promoted apoptosis in LPMCs in vivo. Interestingly, triptolide significantly induced the apoptosis of LP-CD4-positive but not LP-CD4-negative cells. Triptolide significantly induced SOCS3 protein and reduced STAT3 target anti-apoptotic genes Bcl-2 and Bcl-xl in LPMCs. The results were confirmed by an in vitro study using colonic explants cultured with triptolide. Conclusions Our results indicated that triptolide therapy may restore the homeostatic balance of LP-T cell apoptosis within the gut, and demonstrate a novel mechanism of action of triptolide therapy mediated through regulation IL-6/STAT3/SOCS3 signaling pathway. © 2013 Elsevier B.V.

Pan J.,Anhui Medical University | Chen M.,Anhui Medical University | Zhang X.,First Peoples Hospital of Hefei | Chen Y.,First Peoples Hospital of Hangzhou | And 2 more authors.
Indian Journal of Dermatology | Year: 2012

Objectives: This study sought to determine the high risk factors for severe hand, foot, and mouth disease (HFMD). Materials and Methods: Retrospective 229 severe HFMD cases from four hospitals in FuYang, HeFei, and BoZhou (Anhui Provincial Hospital, Fuyang City People's Hospital, No. 2 People's Hospital of Fuyang and Bozhou city People's Hospital) in 2008-2009 were studied, with 140 mild HFMD cases in the same area. Using univariate and multivariate logistic regression analyses, the high risk factors of HFMD were identified by comparing clinical and laboratory findings between severe cases and mild cases. Results: There was a significant difference in age, total duration of fever, rate of respiratory and heart, shake of limbs, white blood cell count, blood sugar, and CK-MB between the two groups. Univariate logistic regression analysis showed that severe cases were associated with age (<3 years), withdrawnness and lethargy, shake of limbs, tachycardia, total leukocyte count (1710 9 /l), blood sugar (7 mmol/l), and CK-MB (16 mmol/l). Furthermore, age (<3 years), withdrawnness, and lethargy, shake of limbs, WBC (1710 9 /l), and CK-MB (16 mmol/l) were found to be high risk factors for severe cases after multivariate logistic regression analysis. Conclusions: Clinicians should give importance to these risk factors. Early recognition of children at risk and timely intervention is the key to reduce acute mortality and morbidity.

Wang T.,Anhui Medical University | Wang T.,First Peoples Hospital of Hefei | Yan X.-B.,Anhui Medical University | Zhao J.-J.,First Hospital of Jiande | And 5 more authors.
Lung Cancer | Year: 2011

Lung cancer is currently the leading cause of cancer-related death in the world. Signal transducers and activators of transcription 3 (STAT3) is a major oncogenic transcription factor involved in the development and progression of a number of human tumors including lung denocarcinoma. Gene associated with retinoid-interferon-induced mortality-19 (GRIM-19) is known to functionally interact with STAT3 and inhibit its transcriptional activity. Decreased expression of GRIM-19 has been reported in tumors including those from kidney, prostate, colon and cervix, indicating that loss of GRIM-19 may be involved in the tumorigenesis through activation of the STAT3 pathway. In this study, we determined that GRIM-19 was significantly reduced at the mRNA and protein levels in lung adenocarcinoma tissues. Moreover, STAT3 was increased in these tumors and corresponding changes in the expression of its downstream target genes was observed. Overexpression of GRIM-19 was also found to suppress lung adenocancinoma tumor growth both in vitro and in vivo. Taken together, these findings will likely contribute to the future development of GRIM-19-based gene therapy approaches to treat lung adenocancinoma. © 2010 Elsevier Ireland Ltd.

Chen P.,Anhui University of Science and Technology | Chen P.,Chinese Academy of Sciences | Li J.,Fuzhou General Hospital of Nanjing Command | Ma J.,First Peoples Hospital of Hefei | And 4 more authors.
IUBMB Life | Year: 2013

Phosphoribosyl pyrophosphate synthetase isoform 1 (PRS1) has an essential role in the de novo and salvage synthesis of human purine and pyrimidine nucleotides. The dysfunction of PRS1 will dramatically influence nucleotides' concentration in patient's body and lead to different kinds of disorders (such as hyperuricemia, gout and deafness). The D52H missense mutation of PRS1 will lead to a conspicuous phosphoribosyl pyrophosphate content elevation in the erythrocyte of patients and finally induce hyperuricemia and serious gout. In this study, the enzyme activity analysis indicated that D52H-mutant possessed similar catalytic activity to the wild-type PRS1, and the 2.27 A resolution D52H-mutant crystal structure revealed that the stable interaction network surrounding the 52 position of PRS1 would be completely destroyed by the substitution of histidine. These interaction variations would further influence the conformation of ADP-binding pocket of D52H-mutant and reduced the inhibitor sensitivity of PRS1 in patient's body. © 2013 IUBMB Life.

Cheng Y.H.,Nanjing University of Traditional Chinese Medicine | Cheng Y.H.,First Peoples Hospital of Hefei | Huang G.C.,Nanjing University of Traditional Chinese Medicine
Evidence-based Complementary and Alternative Medicine | Year: 2014

Objective. To systematically evaluate the evidence of whether massage therapy (MT) is effective for neck pain. Methods. Randomized controlled trials (RCTs) were identified through searches of 5 English and Chinese databases (to December 2012). The search terms included neck pain, neck disorders, cervical vertebrae, massage, manual therapy, Tuina, and random. In addition, we performed hand searches at the library of Nanjing University of Traditional Chinese Medicine. Two reviewers independently abstracted data and assessed the methodological quality of RCTs by PEDro scale. And the meta-analyses of improvements on pain and neck-related function were conducted. Results. Fifteen RCTs met inclusion criteria. The meta-analysis showed that MT experienced better immediate effects on pain relief compared with inactive therapies (n = 153; standardised mean difference (SMD), 1.30; 95% confidence interval (CI), 0.09 to 2.50; P = 0.03) and traditional Chinese medicine (n = 125; SMD, 0.73; 95% CI 0.13 to 1.33; P = 0.02). There was no valid evidence of MT on improving dysfunction. With regard to follow-up effects, there was not enough evidence of MT for neck pain. Conclusions. This systematic review found moderate evidence of MT on improving pain in patients with neck pain compared with inactive therapies and limited evidence compared with traditional Chinese medicine. There were no valid lines of evidence of MT on improving dysfunction. High quality RCTs are urgently needed to confirm these results and continue to compare MT with other active therapies for neck pain. © 2014 Yong Hong Cheng and Gui Cheng Huang.

Lei Y.,Anhui Medical University | Li H.-X.,First Peoples Hospital of Hefei | Jin W.-S.,Anhui Medical University | Peng W.-R.,Anhui Medical University | And 5 more authors.
International Journal of Radiation Biology | Year: 2013

Purpose: To investigate the radiosensitizing effect and mechanism of action by the natural product Paeonol on lung adenocarcinoma both in vitro and in vivo. Materials and methods: Two lung adenocarcinoma cell lines (human lung adenocarcinoma cell line A549 and mouse Lewis lung carcinoma (LLC) cell line) were chosen for this research. In order to select the experimental concentrations of Paeonol, cytotoxicity was determined using a MTT (3-[4,5-dimethylthiazol-2-yl]-2,5- diphenyltetrazolium bromide) assay. A clonogenic assay was performed to measure the radiosensitizing effects. Apoptosis was determined by the Tunel (terminal deoxynucleotidyl transferase-mediated dUTP nick and labeling) assay and flow cytometry. Protein expression was analyzed by Western blotting. To test the radiosensitizing effect in vivo, a transplanted tumor model was established. Results: The MTT assay showed that Paeonol inhibited proliferation of cells. Paeonol concentration ranged from an IC5 (5% inhibiting concentration) to an IC20 and was used at non-toxic concentrations for subsequent experiments. The clonogenic assay showed that Paeonol enhanced the radiosensitivity of cells. Data from the Tunel assay and flow cytometry verified that Paeonol enhanced radiation-induced apoptosis. Paeonol inhibited the activation of the PI3K/AKT (Phosphatidylinositol 3-kinase/ Protein Kinase B) pathway and down-regulated the expression of COX-2 (Cyclooxygenase-2) and Survivin. Paeonol (1718 mg/kg) combined with 10 Gy irradiation inhibited the growth of a transplanted tumor model in vivo, resulting in the longest tumor growth time, tumor growth delay and the highest inhibition ratio when compared with the radiotherapy alone group. Conclusions: It is reported for the first time that Paeonol has a radiosensitizing effect on lung adenocarcinoma both in vitro and in vivo. This effect could be related to the augmentation of radiation-induced apoptosis and the inhibition of the PI3K/Akt signalling pathway and its downstream proteins: COX-2 and Survivin. © 2013 Informa UK, Ltd.

Zheng X.,Anhui University of Science and Technology | Cheng M.,Anhui University of Science and Technology | Cheng M.,Anhui Medical University | Fu B.,Anhui University of Science and Technology | And 6 more authors.
Cancer Research | Year: 2015

There remains a great need for effective therapies for lung cancer, the majority of which are non-small cell lung cancers (NSCLC). Here, we report the identification of a novel candidate therapeutic target, LUNX, as a molecule overexpressed in primary NSCLC and lymph node metastases that is associated with reduced postoperative survival. Functional studies demonstrated that LUNX overexpression promoted lung cancer cell migration and proliferation by interactions with the chaperone protein 14-3-3. Conversely, LUNX silencing disrupted primary tumor growth, local invasion, and metastatic colonization. The finding that LUNX was expressed on cell membranes prompted us to generate and characterize LUNX antibodies as a candidate therapeutic. Anti-LUNX could down-regulate LUNX and reduce lung cancer cell proliferation and migration in vitro. Administered in vivo to mice bearing lung cancer xenografts, anti-LUNX could slow tumor growth and metastasis and improve mouse survival. Together, our work provides a preclinical proof of concept for LUNX as a novel candidate target for immunotherapy in lung cancer. ©2015 AACR.

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