Linzi District Peoples Hospital
Linzi District Peoples Hospital
Guo Y.-X.,Taishan Medical University |
Liu L.,Linzi District Peoples Hospital |
Yan D.-Z.,Linqing City Peoples Hospital |
Guo J.-P.,Third Peoples Hospital of Chongqing
Molecular Medicine Reports | Year: 2017
Osteoarthritis (OA) is an inflammatory disorder dealing with the focal degradation of articular cartilage. Oxidative stress and inflammation are the major events in OA. The present study aimed at identifying the mechanism of the potent antioxidant, plumbagin, in protecting against hydrogen peroxide (H2O2)-induced chondrocyte oxidative stress and inflammatory signaling. Oxidative stress was determined by measuring reactive oxygen species, lipid peroxidation, non-enzymic (glutathione; GSH) and enzymic antioxidant activities (GSH, glutathione S-transferase, glutathione peroxidase, superoxide dismutase, catalase). Expression levels of nuclear factor (erythroid-derived 2)-like 2 (Nrf-2), heme oxygenase 1 (HO-1), NAD(P)H:quinone oxidoreductase 1 (NQO-1), nuclear factor-κB (NF-κB), cyclooxygenase-2 (COX-2) and inducible NO synthase (iNOS) were determined by western blot analysis. Pro-inflammatory cytokine expression levels were assessed using ELISA. Results from reactive oxygen species generation, lipid peroxidation content and antioxidant enzyme activities demonstrated that plumbagin significantly inhibited oxidative stress status in H2O2-induced chondrocytes. In addition, plumbagin modulated transcription factors involved in redox and inflammation regulation, including NF-κB and Nrf-2, by nuclear expression. plumbagin enhanced antioxidant status by increasing the expression levels of Nrf-2 target genes, including HO-1 and NQO-1. An anti-inflammatory effect against chondrocyte-induced inflammation was demonstrated by downregulating COX-2, iNOS and pro-inflammatory cytokine expression levels (tumor necrosis factor-α, interleukin (IL)-6 and IL-8). The present study identified strong evidence for a protective role of plumbagin against H2O2-induced oxidative stress and inflammation in chondrocytes by modulating redox signaling transcription factors.
Gao Y.,Capital Medical University |
Jiang F.,Peking Union Medical College |
Wang X.,Linzi District Peoples Hospital
International Journal of Clinical and Experimental Medicine | Year: 2015
This study is to compare the outcomes of tri-acryl gelatin microspheres (TAGM) and polyvinyl alcohol (PVA) in the treatment of uterine myomas with uterine artery embolization (UAE). Meta-analysis was performed by electronic literature searches from databases including Cochrane Central Register of Controlled Trials, PubMed, EMBASE and meta Register of Controlled Trials for studies published prior to December 2014. Randomized controlled trials comparing TAGM and PVA treating uterine myomas were included in the analysis. Information retrieved from each study included study design, number of participants, study settings, patient characteristics, sample size, follow-up duration and outcomes. Imaging outcomes and clinical outcomes were the main criteria for the evaluation of the included studies. Twenty-eight articles published from 1966 to December 2014 were retrieved through database searching and other sources. After initial screening and assessment, five randomized controlled trials, including 309 women with uterine myomas, met the inclusion criteria. In both imaging and clinical outcomes, TAGM group showed superior or similar effects than PVA group. The results showed more number of patients with significant tumor enhancement, greater mean change in tumor volume, greater mean changes in symptom score and QOL score in TAGM group compared with PVA group, with significant differences. TAGM and PVA groups had similar uterine volume, mean changes in bleeding score and pain score. TAGM is better than PVA as an embolic agent in the treatment of uterine myomas with UAE. © 2015, E-Century Publishing Corporation. All rights reserved.
Yu X.-D.,Taizhou Municipal Hospital |
Yang R.,Linzi District Huangcheng Town Health Center |
Leng C.-J.,Linzi District Peoples Hospital
Computational Biology and Chemistry | Year: 2016
Human epidermal growth factor receptor (EGFR) plays a central role in the pathological progression and metastasis of lung cancer; the development and clinical application of therapeutic agents that target the receptor provide important insights for new lung cancer therapies. The tumor-suppressor protein MIG6 is a negative regulator of EGFR, which can bind at the activation interface of asymmetric dimer of EGFR kinase domains to disrupt dimerization and then inactivate the kinase (Zhang X. et al. Nature 2007, 450: 741-744). The protein adopts two separated segments, i.e. MIG6segment 1 and MIG6segment 2, to directly interact with EGFR. Here, computational modeling and analysis of the intermolecular interaction between EGFR kinase domain and MIG6segment 2 peptide revealed that the peptide is folded into a two-stranded β-sheet composed of β-strand 1 and β-strand 2; only the β-strand 2 can directly interact with EGFR activation loop, while leaving β-strand 1 apart from the kinase. A C-terminal island within the β-strand 2 is primarily responsible for peptide binding, which was truncated from the MIG6segment 2 and exhibited weak affinity to EGFR kinase domain. Structural and energetic analysis suggested that phosphorylation at residues Tyr394 and Tyr395 of truncated peptide can considerably improve EGFR affinity, and mutation of other residues can further optimize the peptide binding capability. Subsequently, three derivative versions of the truncated peptide, including phosphorylated and dephosphorylated peptides as well as a double-point mutant were synthesized and purified, and their affinities to the recombinant protein of human EGFR kinase domain were determined by fluorescence anisotropy titration. As expected theoretically, the dephosphorylated peptide has no observable binding to the kinase, and phosphorylation and mutation can confer low and moderate affinities to the peptide, respectively, suggesting a good consistence between the computational analysis and experimental assay. © 2016 Elsevier Ltd. All rights reserved.
PubMed | Taizhou Municipal Hospital, Linzi District Peoples Hospital and Linzi District Huangcheng Town Health Center
Type: | Journal: Computational biology and chemistry | Year: 2016
Human epidermal growth factor receptor (EGFR) plays a central role in the pathological progression and metastasis of lung cancer; the development and clinical application of therapeutic agents that target the receptor provide important insights for new lung cancer therapies. The tumor-suppressor protein MIG6 is a negative regulator of EGFR, which can bind at the activation interface of asymmetric dimer of EGFR kinase domains to disrupt dimerization and then inactivate the kinase (Zhang X. et al. Nature 2007, 450: 741-744). The protein adopts two separated segments, i.e. MIG6(segment 1) and MIG6(segment 2), to directly interact with EGFR. Here, computational modeling and analysis of the intermolecular interaction between EGFR kinase domain and MIG6(segment 2) peptide revealed that the peptide is folded into a two-stranded -sheet composed of -strand 1 and -strand 2; only the -strand 2 can directly interact with EGFR activation loop, while leaving -strand 1 apart from the kinase. A C-terminal island within the -strand 2 is primarily responsible for peptide binding, which was truncated from the MIG6(segment 2) and exhibited weak affinity to EGFR kinase domain. Structural and energetic analysis suggested that phosphorylation at residues Tyr394 and Tyr395 of truncated peptide can considerably improve EGFR affinity, and mutation of other residues can further optimize the peptide binding capability. Subsequently, three derivative versions of the truncated peptide, including phosphorylated and dephosphorylated peptides as well as a double-point mutant were synthesized and purified, and their affinities to the recombinant protein of human EGFR kinase domain were determined by fluorescence anisotropy titration. As expected theoretically, the dephosphorylated peptide has no observable binding to the kinase, and phosphorylation and mutation can confer low and moderate affinities to the peptide, respectively, suggesting a good consistence between the computational analysis and experimental assay.
PubMed | Yantai Yuhuangding Hospital, Zhucheng Peoples Hospital, Qingdao municipal hospital, Qingdao University and Linzi District Peoples Hospital
Type: Journal Article | Journal: Oncotarget | Year: 2016
The molecular biological mechanisms underlying the evolutionary biologic changes leading to carcinogenesis remain unclear. The main objective of our study was to explore the evolution of the microbiota community and molecules related with CRC in the dynamic transition from normal colon epithelium to premalignant adenoma with the aid of an adenoma-carcinoma sequence mouse CRC model induced by DMH. We generated a modified mouse CRC model induced by DMH for DNA sequences, and characterized the molecular networks. Data from 454 pyrosequencing of the V3- V5 region of the 16S rDNA gene and immunohistochemical detection of APC, P53, K-RAS and BRAF genes were assessed with Principal coordinates, UniFrac, and Kruskal-Wallis rank sum test. The inflammatory group showed enrichment of Bacteroidetes and Porphyromonadaceae (P < 0.01). OTUs affiliated with Firmicutes were enriched in the hyperproliferative group (P < 0.01). Rikenellaceae and Ruminococcaceae showed an increasing trend during the CRC process while the opposite pattern was observed for Prevotellaceaeand Enterobacteriaceae. OTUs related to Alistipes finegoldii were significantly increased during CRC development, P53, K-RAS and BRAF, were gradually increased (P < 0.05). Conversely, expression of APC was decreased during the course of development of CRC. Our results demonstrate that the biological evolutionary shift of gut microbiota, characterized by a gradual decrease in driver bacteria and an increase in DNA damage-causing bacteria, is accompanied by tumor development in the CRC model. The synergistic actions of microbiota dysbiosis and effects of bacterial metabolites on related molecular events are proposed to contribute to the progression of CRC tumorigenesis.
Shang H.,Shandong University |
Shang H.,General Hospital of Zibo |
Wang T.,Linzi District Peoples Hospital |
Shang F.,Chinese People's Liberation Army |
And 2 more authors.
Molecular Medicine Reports | Year: 2014
MicroRNAs (miRNAs) are small non-coding RNAs that inhibit the expression of target protein-coding genes, most often at the post-transcriptional level. miRNAs are often found to be misregulated in human cancer and they can act as potent oncogenes or tumor suppressor genes. In this study, we found that a germline mutation in the miR-125a coding region is associated with human gastric cancer. This mutation reduced the expression of mature miR-125a and alleviated its inhibitory effect on erythroblastic leukemia viral oncogene homolog 2 (ERBB2) gene expression and on gastric tumor cell proliferation. Thus, the data of this study suggested that this germline mutation in pri-miR-125a likely contributes to the genetic predisposition to gastric cancer by reducing the production of miR-125a, thereby interfering with the expression of miR-125a target genes.
Zhang X.-M.,Shandong University |
Shan N.-N.,Shandong University |
Sun M.,Linzi District Peoples Hospital |
Wang X.,Shandong University |
And 5 more authors.
International Immunopharmacology | Year: 2014
Background The T-cell immunoglobulin and mucin domain-(Tim)-1 molecule and Tim-3 are mainly expressed on activated T helper (Th) 2 and Th1 cells, respectively, and have been implicated in the pathogenesis of some autoimmune diseases. Immune thrombocytopenia (ITP) is a common autoimmune disorder, and the complex dysregulation of cellular immunity has been observed; however, the relationship between Tims and excessive immune responses in ITP remains unclear. Methods Using real-time quantitative polymerase chain reaction (RT-PCR), the mRNA expression levels of Tim-1, Tim-3, T-box transcription factor (T-bet) and GATA binding protein 3 (GATA-3) were measured in the peripheral blood mononuclear cells (PBMCs) of 45 newly diagnosed patients with active ITP, 34 ITP patients in remission and 31 healthy volunteers. Results Tim-3 mRNA expression in PBMCs in newly diagnosed patients was significantly decreased. At the same time, Tim-1 mRNA was not significantly declined, which resulted in a decreased ratio of Tim-3 to Tim-1 in ITP patients with active disease. During the remission stages, the levels of these transcription factors were comparable with those observed in healthy controls. Conclusions The reduced levels of Tim-3/Tim-1 in PBMCs during active stages of the disease suggest a possible role in the pathogenesis and course of ITP. Regulating the balance of Tim-1 and Tim-3 in ITP patients could also be a therapeutic approach against ITP. © 2013 Elsevier B.V.
Zhang S.-L.,Linzi District Peoples Hospital |
Liu L.,Central South University
Experimental and Therapeutic Medicine | Year: 2015
microRNA (miR)-148a has been shown to act as an important suppressor in numerous human malignancies and is markedly downregulated in hepatocellular carcinoma; however, the role of miR-148a in the regulation of hepatocellular carcinoma cell invasion, as well as the underlying mechanism, has never been studied. In the present study, the expression level of miR-148a was found to be significantly decreased in hepatocellular carcinoma tissues and HepG2 cells when compared with that in the normal adjacent tissues. Furthermore, a novel target of miR-148a was found, sphingosine-1-phosphate receptor 1 (S1PR1), whose expression was negatively regulated by miR-148a at a post-transcriptional level in hepatocellular carcinoma HepG2 cells. Upregulation of miR-148a by transfection with miR-148a mimics notably suppressed HepG2 cell invasion, similar to the effect of the SIPR1 downregulation induced by SIPR1-specific small interfering RNA, while the restoration of S1PR1 expression reversed the inhibitory effect of miR-148a upregulation on HepG2 cell invasion. Accordingly, the current study suggests that miR-148a plays an inhibitory role in the regulation of hepatocellular carcinoma cell invasion by directly targeting S1PR1. © 2014, Spandidos Publications. All rights reserved.
PubMed | Linzi District Peoples Hospital
Type: Journal Article | Journal: Journal of Korean medical science | Year: 2016
To investigate the function and regulation mechanism of ATP-binding cassette, subfamily G, member 2 (ABCG2) in retinoblastoma cancer stem cells (RCSCs), a long-term culture of RCSCs from WERI-Rb1 cell line was successfully established based on the high expression level of ABCG2 on the surface of RCSCs. To further explore the molecular mechanism of ABCG2 on RCSCs, a microRNA that specifically targets ABCG2 was predicted. Subsequently, miR-3163 was selected and confirmed as the ABCG2-regulating microRNA. Overexpression of miR-3163 led to a significant decrease in ABCG2 expression. Additionally, ABCG2 loss-of-function induced anti-proliferation and apoptosis-promoting functions in RCSCs, and multidrug resistance to cisplatin, carboplatin, vincristine, doxorubicin, and etoposide was greatly improved in these cells. Our data suggest that miR-3163 has a significant impact on ABCG2 expression and can influence proliferation, apoptosis, and drug resistance in RCSCs. This work may provide new therapeutic targets for retinoblastoma.
Jing X.-H.,Linzi District Peoples Hospital |
Song C.-Y.,Weifang Medical University
International Eye Science | Year: 2014
AIM: To investigate the clinical efficacy and safety of intravitreal injection of triamcinolone combined macular grid photocoagulation treatment for macular edema.METHODS: Totally 150 cases (150 eyes) with macular edema in our hospital from July 2009 to November 2013 were selected, which were randomly divided into study group (75 cases, 75 eyes) and control group (75 cases, 75 eyes). The cases in control group were treated with macular grid photocoagulation treatment, those in the study group used triamcinolone acetonide combined macular grid photocoagulation treatment. Best corrected visual acuity (BCVA), parallel optical coherence tomography (OCT) and fundus fluorescein angiography (FFA) were detected before treatment, after treatment 7d, 1, 3, and 9mo.RESULTS: After the treatment, patients' vision were significantly improved in two groups (P<0.05). In the study group 7d, 1, 3, and 9mo after operation, the visual acuity was better than the control group and preoperative (P<0.05); fovea macular neurosensory layer thickness decreased significantly (P<0.05). In the control group, the point omentum macular neurosensory retinal thickness was not statistically significant at 7d, 1, 3, and 9mo after operation compared with before treatment (P>0.05). Fovea macular neurosensory retinal thickness in the study group was significantly lower than that in control group (P<0.05). Intraocular pressure of 7 cases in the study group increased slightly, and were normal after treatment.CONCLUSION: Triamcinolone acetonide combined macular grid photocoagulation treatment is accurate, can effectively improve the visual acuity, reduce macular edema, it is safe and reliable, and suitable for clinical application.