The Peoples Hospital of Bozhou

Bozhou, China

The Peoples Hospital of Bozhou

Bozhou, China
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Wang Y.,Binzhou Medical University | Wang Y.,The Peoples Hospital Of Bozhou | Ma J.,Binzhou Medical University | Yan X.,Shihezi University | And 6 more authors.
Recent Patents on Anti-Cancer Drug Discovery | Year: 2016

Background: Isoliquiritigenin (ISL) is a licorice chalcone. According to CN104758274, CN101658513 and US009089546, it is claimed that ISL has anti-inflammatory, anti-oxidative, and anti-tumoral effects. Objective: This study aimed to investigate the potential therapeutic effect of ISL in mouse melanoma B16F10 cells. Methods: Sulforhodamine B (SRB) colorimetric assay was used to test the effects of ISL on proliferation. Commercial assay kits were applied to assess glucose uptake, lactate production and ATP levels. Measurement of apoptosis was involved with Hoechst 33258, JC-1 and annexin V-FITC/PI staining. H2DCFDA probe was employed to detect ROS generation. Quantitative RT-PCR and western blot were utilized to measure the mRNA and protein levels. Results: ISL abated hypoxia-inducible factor 1α (HIF-1α) stability and reduced a series of glycolysis-relevant enzymes expression, including glucose transporters 1/4 (GLUT 1/4), hexokinase 2 (HK2), pyruvate kinase M2 (PKM2) and lactate dehydrogenase A (LDHA). Exposure to ISL induced the mitochondrial membrane potential depolarization and increased intracellular reactive oxygen species (ROS) level. ISL could effectively inhibit proliferation and alleviate hypoxia in mouse melanoma B16F10 cells via inducing apoptosis and reducing the expression of significant enzymes in the glycolysis. ISL significantly inhibited B16F10 cell proliferation via inducing apoptosis, and alleviated hypoxia by recovering mitochondrial function and reversing high glycolysis. Conclusion: Our findings propose that ISL can be a promising therapeutic agent for the melanoma via reliving hypoxia of microenvironment and targeting energy metabolism system of cancer cells. Consistent with WO2015079213 and WO2014084494, targeting glycolysis can be an effective means to anti-cancer. © 2016 Bentham Science Publishers.


PubMed | The Peoples Hospital of Bozhou and Shanghai JiaoTong University
Type: Journal Article | Journal: Molecular medicine reports | Year: 2015

Gene expression profiles of samples taken from patients with acute lung injury (ALI) induced by mechanical ventilation (MV) and lipopolysaccharide (LPS) were analyzed in order to identify key genes, and explore the underlying mechanisms. The GSE2411 microarray data set was downloaded from the Gene Expression Omnibus. This data set contained microarray data from 24 mouse lung samples, which were equally divided into four groups: Control group, MV group, LPS group and MV+LPS group. Differentially expressed genes (DEGs) were identified in the MV, LPS and MV+LPS groups, as compared with the control group, using packages of R software. Hierarchical clustering and betweengroup comparisons were performed for each group of DEGs. Overrepresented biological processes were revealed by functional enrichment analysis using the Database for Annotation, Visualization and Integrated Discovery. Unique DEGs in the LPS and MV+LPS groups were selected, and pathway enrichment analyses were performed using the Kyoto Encyclopedia of Genes and Genomes Orthology Based Annotation system. A total of 32, 264 and 685 DEGs were identified in the MV, LPS and MV+LPS groups, respectively. The MV+LPS group had more DEGs, as compared with the other two treatment groups. Genes associated with the immune and inflammatory responses were significantly overrepresented in both the LPS and MV+LPS groups, suggesting that LPS dominated the progression of ALI. Unique DEGs in the LPS and MV+LPS groups were associated with cytokinecytokine receptor interaction. The Janus kinasesignal transducer and activator of transcription signaling pathway was shown to be enriched in the LPS+MVunique DEGs. The results of the present study demonstrated that MV could exaggerate the transcriptional response of the lungs to LPS. Numerous key genes were identified, which may advance knowledge regarding the pathogenesis of ALI.


PubMed | The Peoples Hospital of Bozhou and Fujian Medical University
Type: | Journal: Journal of immunology research | Year: 2015

Mesenchymal stem cells are immunoregulation cells. IL-22 plays an important role in the pathogenesis of immune thrombocytopenia. However, the effects of mesenchymal stem cells on IL-22 production in patients with immune thrombocytopenia remain unclear. Flow cytometry analyzed immunophenotypes of mesenchymal stem cells; differentiation of mesenchymal stem cells was observed by oil red O and Alizarin red S staining; cell proliferation suppression was measured with MTS; IL-22 levels of cell-free supernatants were determined by ELISA. Mesenchymal stem cells inhibited the proliferation of activated CD4(+)T cells; moreover, mesenchymal stem cells immunosuppressed IL-22 by soluble cellular factors but not PGE2. These results suggest that mesenchymal stem cells may be a therapeutic strategy for patients with immune thrombocytopenia.


Lin D.,Soochow University of China | Liu C.,Soochow University of China | Xue M.,Soochow University of China | Liu R.,Soochow University of China | And 9 more authors.
PLoS ONE | Year: 2010

Background: Interleukin-15 (IL-15) plays important roles in the immune system and in the development of hematopoietic cells. Previous studies revealed that five SNPs in IL-15, rs10519612, rs10519613, rs35964658, rs17007695 and rs17015014, were significantly associated with childhood Acute Lymphoblastic Leukemia (ALL) treatment response. In adult ALL, the expression of IL-15 was also correlated with the immunophenotypes of ALL. Therefore, we hypothesize that SNPs of IL-15 might also be associated with adult ALL. Methods and Findings: We genotyped the above five SNPs of IL-15 gene by PCR-RFLP assays in adult ALL case-control studies. The current study included 121 adult ALL patients and 263 healthy controls. IL-15 genotypes and haplotypes were determined and the associations with the risk of ALL were analyzed by logistic regression. SNPs rs10519612 and rs17007695 were significantly associated with ALL (P = 0.013 and P = 0.001). We observed a 2-fold and 2.4-fold excess risk of developing ALL for the rs10519612 CC and rs17007695 TC genotype carriers compared with non-carriers, respectively. Haplotype analysis revealed that haplotypes ACAC, CAGT and CCAT were significantly associated with adult B-ALL, while haplotype CCAT conferred susceptibility to T-ALL. Conclusion: These findings suggest that IL-15 gene polymorphisms are significantly associated with ALL in adult Chinese population. ©2010 Lin et al.


Rong L.,The Peoples Hospital Of Bozhou | Rong L.,Anhui University of Science and Technology | Hu D.,The Peoples Hospital Of Bozhou | Wang W.,The Peoples Hospital Of Bozhou | And 3 more authors.
Biomedical Research (India) | Year: 2016

To study the chemical constituents of Stephania kwangsiensis Lo. and to explore the effects of corydine on proliferation and apoptosis of lung adenocarcinoma NCI-H446 cells. Chemical structures were elucidated by MS, 1H-NMR and 13C-NMR. Effects of different concentrations of corydine on proliferation of lung adenocarcinoma NCI-H446 cells were determined by MTT assay. Effects of corydine on apoptosis rate of NCI-H446 cells were determined by flow cytometry. Three types of alkaloids were isolated from root tubers of Menispermaceae Stephania plant Stephania kwangsiensis Lo. Three different concentrations of corydine (20, 10, 5 Lg/ml) could all significantly increase the apoptosis rate of NCI-H446 cells after 48 h of treatment compared to the control group. Corydine can inhibit the proliferation of lung cancer NCI-H446 cells and induce their apoptosis. © 2016, Scientific Publishers of India. All rights reserved.


Chai P.,The Peoples Hospital of Bozhou | Tian J.,The Peoples Hospital of Bozhou | Zhao D.,The Hospital of Suzhou | Zhang H.,The Peoples Hospital of Bozhou | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2016

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p. © 2016.


Li X.,The Peoples Hospital of Bozhou | Wang Y.,The Peoples Hospital of Bozhou | Wang H.,The Peoples Hospital of Bozhou | Huang C.,The Peoples Hospital of Bozhou | And 2 more authors.
Inflammation research : official journal of the European Histamine Research Society ... [et al.] | Year: 2015

OBJECTIVE: The objective of the review is to examine the crossroads of autophagy, inflammation, and apoptosis signaling pathways and their participation in liver fibrosis.INTRODUCTION: Endoplasmic reticulum (ER) stress was emerged as a common feature relevant to the pathogenesis of diseases associated with organ fibrosis. However, the functional consequences of these alterations on ER stress and the possible involvement in liver fibrosis were currently largely unexplored. Here, we will survey the recent literature in the field and discuss recent insights focusing on some cellular models expressing mutant proteins involved in liver fibrosis.METHODS: A computer-based online search with PubMed, Scopus and Web of Science databases was performed for articles published, concerning ER stress, adaptation, inflammation and apoptosis with relevance to liver fibrosis.RESULTS AND CONCLUSIONS: Progression of liver fibrosis requires sustained inflammation leading to hepatocytes apoptosis through ER stress, whereas associated with activation of hepatic stellate cells (HSCs) into a fibrogenic and proliferative cell type. Faced with persistent and massive ER stress, HSCs adaptation starts to fail and apoptosis occurs in reversal of liver fibrosis, possibly mediated through calcium perturbations, unfolded protein response, and the pro-apoptotic transcription factor CHOP. Although limited in scope, current studies underscored that ER stress is tightly linked to adaptation, inflammation and apoptosis, and recent evidences suggested that these processes are related to the pathogenesis of liver fibrosis and its recovery.


PubMed | The Hospital of Suzhou, The Peoples Hospital of Bozhou and Anhui Medical University
Type: Journal Article | Journal: Biochemical and biophysical research communications | Year: 2016

Gse1 coiled-coil protein (GSE1), also known as KIAA0182, is a proline rich protein. However, the function of GSE1 is largely unknown. In this study, we reported that GSE1 is overexpression in breast cancer and silencing of GSE1 significantly suppressed breast cancer cells proliferation, migration and invasion. Furthermore, GSE1 was identified as a direct target of miR-489-5p, which is significantly reduced in breast cancer tissues. In addition, forced expression of miR-489-5p suppressed breast cancer cells proliferation, migration and invasion. Moreover, depletion of GSE1 by siRNAs significantly abrogated the enhanced proliferation, migration and invasion of breast cancer cells consequent to miR-489-5p depletion. Taken together, these findings suggest that GSE1 may function as a novel oncogene in breast cancer and it can be regulated by miR-489-5p.


PubMed | The Peoples Hospital of Bozhou
Type: Journal Article | Journal: Inflammation research : official journal of the European Histamine Research Society ... [et al.] | Year: 2015

The objective of the review is to examine the crossroads of autophagy, inflammation, and apoptosis signaling pathways and their participation in liver fibrosis.Endoplasmic reticulum (ER) stress was emerged as a common feature relevant to the pathogenesis of diseases associated with organ fibrosis. However, the functional consequences of these alterations on ER stress and the possible involvement in liver fibrosis were currently largely unexplored. Here, we will survey the recent literature in the field and discuss recent insights focusing on some cellular models expressing mutant proteins involved in liver fibrosis.A computer-based online search with PubMed, Scopus and Web of Science databases was performed for articles published, concerning ER stress, adaptation, inflammation and apoptosis with relevance to liver fibrosis.Progression of liver fibrosis requires sustained inflammation leading to hepatocytes apoptosis through ER stress, whereas associated with activation of hepatic stellate cells (HSCs) into a fibrogenic and proliferative cell type. Faced with persistent and massive ER stress, HSCs adaptation starts to fail and apoptosis occurs in reversal of liver fibrosis, possibly mediated through calcium perturbations, unfolded protein response, and the pro-apoptotic transcription factor CHOP. Although limited in scope, current studies underscored that ER stress is tightly linked to adaptation, inflammation and apoptosis, and recent evidences suggested that these processes are related to the pathogenesis of liver fibrosis and its recovery.


PubMed | Jiangsu University and The Peoples Hospital of Bozhou
Type: Journal Article | Journal: PloS one | Year: 2014

Circulating microRNAs (miRNAs), which are extremely stable and protected from RNAse-mediated degradation in body fluids, have emerged as candidate biomarkers for many diseases. The present study aimed to identify a serum microRNA (miRNA) expression profile that could serve as a novel diagnostic biomarker for primary biliary cirrhosis (PBC).Serum miRNA expression was investigated using four cohorts comprising 380 participants (healthy controls and patients with PBC) recruited between August 2010 and June 2013. miRNA expression was initially analyzed by Illumina sequencing using serum samples pooled from 3 patients and 3 controls. Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) was then used to evaluate the expression of selected miRNAs in a screening set (n=40). A logistic regression model was then constructed using a training cohort (n=192) and validated using another cohort (n=142). The area under the receiver operating characteristic curve (AUC) was used to evaluate diagnostic accuracy.We identified a miRNA panel (hsa-miR-122-5p, hsa-miR-141-3p, and hsa-miR-26b-5p) with a high diagnostic accuracy for PBC (AUC=0.905, 95% confidence interval (CI)=0.857 to 0.953; sensitivity=80.5%, specificity=88.3%). There was a significant difference between AUC values of the miRNA panel and those of alkaline phosphatase (ALP) (AUC=0.537, difference between areas=0.314, 95% CI=0.195 to 0.434, P<0.001), and those of antinuclear antibody (ANA) (AUC=0.739, difference between areas=0.112, 95% CI=0.012 to 0.213, P=0.0282).We identified a serum microRNA panel with considerable clinical value in PBC diagnosis. The results indicate that the miRNA panel is a more sensitive and specific biomarker for PBC than ALP and ANA.

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