Time filter

Source Type

Liaocheng, China

Yu X.,Shanghai JiaoTong University | Zhao X.,Liao Cheng Peoples Hospital | Wu T.,Nanjing Medical University | Zhou Z.,Shanghai JiaoTong University | And 3 more authors.
International Orthopaedics | Year: 2013

Purpose: The purpose of this study was to determine the effects of naringin on osteoclastogenesis and osteolysis both in vitro and in vivo. Methods: In this research osteoclasts were generated from mouse bone marrow monocytes with the receptor activator of NF-šB ligand and the macrophage colony stimulating factor. Naringin, at a concentration of 1, 10, 50, and 100 μg/mL, was respectively added to the medium. Seven days later, the osteoclasts were determined through tartrate-resistant acid phosphatase (TRAP) staining. Mature osteoclasts were isolated from newborn rabbits and cultured for three days on bone slices. Naringin at a concentration of 1, 10, 50, and 100 μg/mL was respectively added to the medium. The resorption bone slices were quantified, and the area was calculated after toluidine blue and Mayer-hematoxylin staining. Polymethyl methacrylate (PMMA) particles were implanted on the calvariae of C57BL/J6 mice. Naringin, at a dose of 50 μg/kg and 100 μg/kg, was respectively given intraperitoneally for seven. Seven days later, the calvariae were removed and processed for pathological analysis. Results: The result indicated that naringin treatment effectively inhibited in vitro osteoclastogenesis and inhibited mature osteoclasts. In vivo data indicated that naringin strongly inhibited PMMA-induced osteolysis. Conclusion: Naringin can effectively inhibit osteoclastogenesis and suppress wear particles-induced osteolysis and might be useful in the treatment or prevention of wear particles-induced osteolysis and aseptic loosening for its effect on osteoclast generation and function. © 2012 Springer-Verlag Berlin Heidelberg.

Liu Z.-Z.,Shandong University | Zhao X.-Z.,Liao Cheng Peoples Hospital | Zhang X.-S.,Liao Cheng Peoples Hospital | Zhang M.,Shandong University
International Journal of Clinical and Experimental Pathology | Year: 2014

Researches have shown that the onset of diabetes is closely associated with oxidative stress and the chronic exposure leads to the development of complications such as diabetic cardiomyopathy. One of the central adaptive responses against the oxidative stresses is the activation of the nuclear transcriptional factor, NF-E2-related factor 2 (Nrf2), which then activates more than 20 different antioxidative enzymes. Kelch-like ECH associated protein 1 (Keap1) targets and binds to Nrf2 for proteosomal degradation. The aim of the present study was to investigate the status of Nrf2 mediated antioxidant system in myocardial biopsies of non-diabetic (NDM) and type-2 diabetic (DM-T2) cardiomyopathy patients. The western blot analysis of antioxidant proteins, real-time PCR analysis of Nrf2/Keap1 gene and bisulphate DNA sequencing analysis to study the methylation status of the CpG islands of Keap1 promoter DNA were performed. The immunoblot analysis showed the decreased level of antioxidant proteins other than Keap1 in the diabetic cardiopathy patients. Similarly, mRNA levels of Keap1 showed 5-fold increase in diabetic patients. Further analysis on promoter region of Keap1 gene revealed 80% demethylation in diabetic patients. Altogether, our results indicated that demethylation of the CpG islands in the Keap1 promoter will activate the expression of Keap1 protein, which then increases the targeting of Nrf2 for proteosomal degradation. Decreased Nrf2 activity represses the transcription of many antioxidant enzyme genes and alters the redox-balance up on diabetes. Thus, our study clearly demonstrates the failure of Nrf2 mediated antioxidant system revealed in biopsies of diabetic cardiomyopathy.

Wang L.X.,Liao Cheng Peoples Hospital | Jiang H.L.,Intensive Care Unit | Du S.L.,Liao Cheng Peoples Hospital
Genetics and Molecular Research | Year: 2015

The expression of transforming growth factor-beta 1 (TGF-β1) inside the callus cells of diabetic rats and the impact of insulin therapy on its expression and biomechanics was investigated. The rats were randomly divided as follows: an insulin therapy group (IT), a diabetic model group (DM), and a non-diabetic control group (NC). Bone specimens from each group were extracted at different times for immunohistochemical observation of the expression of TGF-β1. Concurrently, the destruction torque and torsional stiffness were detected at different times. One to four weeks after fracture, TGF-β1 was widely expressed in fractured callus cells and periosteal proliferating cells, while the expression inside diabetic cells was significantly reduced. The expression of TGF-β1 decreased over the first 68 weeks, and the mature bone cells never expressed TGF-β1. The destruction torque (Nm) detected in the 6th week revealed that there was a statistically significant difference between the DM, NC, and IT groups (P < 0.01). In conclusion, TGF-β1 expression was significantly reduced inside the callus cells of diabetic rats. Insulin therapy increased TGF-β1 expression inside the callus cells of diabetic rats and improved the biomechanical characteristics of the callus. © FUNPEC-RP.

Li Q.F.,Liao Cheng Peoples Hospital | Li Q.Y.,Liao Cheng Peoples Hospital | Gao A.R.,Third Hospital of Liaocheng | Shi Q.F.,Liao Cheng Peoples Hospital
Genetics and Molecular Research | Year: 2015

Epigenetic silencing of the GSTP1 gene by promoter methylation has been associated with increased risk and shortened survival in patients with hepatocellular carcinoma (HCC). We therefore conducted a meta-analysis to obtain a more precise estimate of this association. By searching the Cochrane Library, CBM, EMBASE, PubMed, and the Web of Science, we tabulated and analyzed parameters from each study. Results were summarized by meta-analyses using the version 12.0 STATA software. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were also calculated in this analysis. A total of 14 cohort studies (tumor samples = 607, adjacent samples = 356, benign samples = 182, normal samples = 133) were included for the following statistical analysis. Our meta-analysis results demonstrated that the frequency of GSTP1 methylation in cancer tissues was significantly highe than those in adjacent tissues, benign tissues, and normal tissues (all P < 0.05). Further subgroup analysis by country indicated that the frequency of aberrant GSTP1 promoter methylation was correlated to the development of HCC among all the included experimental subgroups (all P < 0.05). The results indicate a significant association between GSTP1 methylation and poor outcomes in HCC patients. ©FUNPEC-RP

Discover hidden collaborations