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.
Yang C.,Linzi District Peoples Hospital |
Wang Y.,Linzi District Peoples Hospital
Surgical Endoscopy and Other Interventional Techniques | Year: 2017
Background: Patients and surgeons are typically satisfied with the cosmetic results of total endoscopic thyroidectomy using the complete areola approach. However, the disadvantages of this approach include an excessive free flap and a longer operative time. Methods: A retrospective analysis was conducted in 72 patients (64 women and 8 men) with a benign thyroid nodule who underwent non-unvisual dissection to establish the operating space for endoscopic surgery. Results: The time needed to create the operating space in the chest was 6.43 ± 0.94 min. The time for the overall operating space was 15.35 ± 1.52 min. The overall surgical time was 96.54 ± 19.32 min. The flap area in the chest was 30.25 ± 3.42 cm2. Conclusions: Application of non-visual dissection shorten the time to create operating space and the overall surgical time, and markedly reduced the flap area. Our non-unvisual dissection technique for establishing the operating space is different from any previous techniques. © 2017 Springer Science+Business Media New York
Yu Y.,Linzi District Peoples Hospital |
Zheng G.,Linzi District Peoples Hospital
Molecular Medicine Reports | Year: 2017
Troxerutin is a bioflavonoid, which can be used to treat venous disorders, thrombosis and cerebrovascular diseases. Recent studies have demonstrated that it may also be used to prevent edemas. However, it is not known whether troxerutin protects against the cardiomyopathic complications of diabetes. In the present study, a rat model of type 2 diabetes was used to investigate the potential for troxerutin to protect against diabetic cardiomyopathy, through changes to nuclear factor-κB (NF-κB) expression. Troxerutin administration significantly reduced heart rate, blood pressure, blood glucose and plasma triglyceride levels across all measured time points. Furthermore, troxerutin significantly reduced reactive oxygen species levels, NF-κB protein expression, and suppressed the phosphorylated forms of AKT, insulin receptor substrate 1 (IRS1) and c-Jun N-terminal kinase (JNK). These results suggested that troxerutin protects against cardiomyopathy via alterations in NF-κB, AKT and IRS1 signaling, in a rat model of type 2 diabetes.
Lv J.,Qingdao University |
Cao M.-Q.,Dongying Peoples Hospital |
Yu J.-C.,Linzi District Peoples Hospital
Bangladesh Journal of Pharmacology | Year: 2015
The aim of the current study was to evaluate the anticancer and apoptotic effects of alantolactone pyrazoline analogue in human non-small cell lung cancer (NCI-H460) cells. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was used to evaluate the cell viability while as fluorescence microscopy was used to assess the effect on apoptosis, cellular and nuclear morphology. Flow cytometry evaluated the effect of APA on cell cycle arrest in these cells. The results revealed that APA induced potent, time and dose-dependent cytotoxic effects on the growth of NCI-H460 cells. It also inhibited colony forming tendency as well as cell invasion capability of these cancer cells. APA induced dose-dependent nuclear and cellular morphological effects including chromatin condensation and DNA fragmentation. Flow cytometry revealed that the anticancer effects of APA might be due to its cell cycle arrest inducing tendency in G0/G1 phase of the cell cycle. © 2015, Bangladesh Pharmacological Society. All right resreved.
Li G.-L.,Linzi District Peoples Hospital |
Li G.-L.,Clinical Laboratory Linzi District Peoples Hospital |
Li Y.-M.,Linzi District Peoples Hospital |
Li Y.-M.,Clinical Laboratory Linzi District Peoples Hospital
International Journal of Surgery | Year: 2017
Objective The aim of the present study was to compare the efficacy and safety of oral tranexamic acid (TXA) with controls or intravenous TXA in patients undergoing total joint arthroplasty (TJA) in a systematic review and meta-analysis. Methods We systematically searched randomized controlled trials (RCTs) from PubMed, Embase, the Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science and Google databases. Any studies comparing oral TXA versus a control group or intravenous TXA for patients prepared for TJA were included. The outcomes included the need for transfusion, hemoglobin drops, length of hospital stay and drain volume. We calculated the risk ratio (RR) with a 95% confidence interval (CI) for the need of transfusion and the weighted mean difference (WMD) with a 95% CI for hemoglobin drop, length of hospital stay and drain blood loss. Stata 12.0 was used for the meta-analysis. Results Five clinical trials (5 RCTs) involving 333 patients were finally included in this meta-analysis. When compared with the control group, oral TXA was associated with less need for transfusion, fewer hemoglobin drops, less drain volume and a shorter length of hospital stay (P < 0.05). When compared with IV TXA, oral TXA was associated with more hemoglobin drops (P < 0.05). However, there was no significant difference between the need for transfusion, drain volume and the length of hospital stay between oral TXA and IV TXA. Conclusion Oral TXA has comparable hemostatic effects with IV TXA and may reduce the costs for patients prepared for TJA. However, considering the limited quality and number of the included studies, more high-quality and multi-center RCTs are still needed to recommend oral TXA for routine administration. © 2017
Qu F.,Jinan Central Hospital |
Wang X.,Linzi District Peoples Hospital
Pharmazie | Year: 2017
Aberrant expression of miR-340 has been found in several kinds of cancers including ovarian cancer. Pro-apoptotic and anti-metastasis roles of miR-340 in ovarian cancer have also been reported; however, the underling molecular mechanisms by which miR-340 suppresses ovarian cancer are still unclear. This study focused on the role and molecular mechanism of miR-340 in ovarian cancer. Human ovarian carcinoma SKOV3 cells were used and transfected with miR-340 mimic, miR-340 inhibitor and their correspondingly negative controls (mimic control and inhibitor control). Thereafter, cell viability, apoptosis, and the expressions of apoptosis-associated factors and BAG3 were respectively assessed by MTT assay, flow cytometry, qRT-PCR and Western blotting. SKOV3 cells were then co-transfected with miR-340 inhibitor and BAG3 targeted siRNA, then cell viability, apoptosis and the expression of apoptosis-associated factors were retested. Besides, the expressions of main factors in PI3K/AKT pathway were detected. Overexpression of miR-340 suppressed BAG3 cells viability (P < 0.05), but improved apoptosis (P < 0.001). BAG3 was negatively regulated by miR-340 (P < 0.05 or P < 0.01). BAG3 silence significantly induced cell apoptosis (P < 0.001), and abolished miR-340 suppression-induced increase in cell viability (P < 0.001). Besides, BAG3 silence abolished miR-340 suppression-induced activation of PI3K and AKT. This study revealed the tumor suppressive role of miR-340 in SKOV3 cells by negative regulation of BAG3. PI3K/AKT pathway might be involved in the regulation of miR-340 and BAG3.
Zhang Z.,Linyi Peoples Hospital |
Huang A.,Linzi District Peoples Hospital |
Zhang A.,Harbin Medical University |
Zhou C.,Changshu No2 Peoples Hospital
Biomedicine and Pharmacotherapy | Year: 2017
HuR, a ubiquitously expressed RNA-binding protein, stabilizes mRNA and regulates its translation. HuR expression was increased at all stages of breast cancer and correlated with poor clinical outcome. However, the detailed mechanisms remain unclear. Here we reported that overexpression of HuR increased CDK3 mRNA stability and thus its protein expression in MDA-MB-231 and MCF-7 cells. Mechanistically, CDK3 mRNA was identified as a target of HuR via bioinformatics and RNA binding protein immunoprecipitation (RIP) assays. Furthermore, treatment with HuR shRNA decreased CDK3 expression, inhibited cell proliferation and promoted cell apoptosis in breast cancer. More importantly, overexpression of CDK3 reversed the suppressive effects of HuR knockdown on cell growth in both MDA-MB-231 and MCF-7 cells. Finally, HuR and CDK3 expression levels were positively correlated and significantly up-regulated in breast cancer samples. And overexpression of HuR attenuated the chemotherapeutical efficiency of breast cancer. Therefore, our results indicate that ectopic expression of HuR promotes breast cancer cell proliferation and survival by directly binding to and stabilizing CDK3 mRNA. © 2017 Elsevier Masson SAS
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.
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 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.