First Hospital of Wuhan
First Hospital of Wuhan
Liu W.,Huazhong University of Science and Technology |
Liu W.,First Hospital of Wuhan |
Zhang Y.,Huazhong University of Science and Technology |
Xia P.,First Hospital of Wuhan |
And 9 more authors.
Biomedicine and Pharmacotherapy | Year: 2016
The precise role of interleukin-1 beta (IL-1β)-induced extracellular matrix degeneration in the pathogenesis of intervertebral disc degeneration (IDD) is currently unknown. Recent evidence has revealed that microRNAs (miRNAs) are associated with IDD, but their function in the extracellular matrix degradation of nucleus pulposus (NP) tissues is also poorly understood. The aim of this study was to evaluate the expression and functional role of miR-7 in IL-1β-induced disc degeneration. The expression level of miR-7 was investigated in degenerative NP tissues and in IL-1β-induced NP cells using quantitative reverse transcription-polymerase chain reaction amplification analysis. A dual-luciferase reporter assay was then utilized to determine whether growth differentiation factor 5 (GDF5) is a target of miR-7. Finally, mRNA and protein levels of known matrix components and of matrix degradation enzymes were determined to elucidate the function of miR-7 in IL-1β-induced disc degeneration. In this study, we found that miR-7 is highly expressed in human degenerative NP tissues and in IL-1β stimulated NP cells compared to normal controls. We also determined that GDF5 was a target of miR-7. Functional analysis showed that the overexpression of miR-7 significantly enhanced the IL-1β-induced extracellular matrix degeneration, whereas inhibition of miR-7 function by antagomiR-7 prevented NP cell detrimental catabolic changes in response to IL-1β. Additionally, the prevention of IL-1β-induced NP extracellular matrix degeneration by miR-7 silencing was attenuated by GDF5 siRNA. These findings suggest that miR-7 contributes to an impaired ECM in intervertebral discs through targeting GDF5 and miR-7 might therefore represent a novel therapeutic target for the prevention of IDD. © 2016 Elsevier Masson SAS
Liu Y.,Huazhong University of Science and Technology |
Li N.,Fujian University of Traditional Chinese Medicine |
Qi Y.-P.,Sun Yat Sen University |
Dai L.,First Hospital of Wuhan |
And 4 more authors.
Advanced Materials | Year: 2011
Phosphorous-based templating analogs of extracellular matrix proteins are used as templates in conjunction with polycarboxylic acid-stabilized amorphous calcium phosphate nanoprecursors to create a highly ordered intrafibrillar apatite crystallite assembly within a collagen fibril. The assembly recapitulates the gap and overlap arrangement of collagen molecules. © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
Yao S.,Wuhan University |
Yao S.,First Hospital of Wuhan |
Zhou J.,First Hospital of Wuhan |
Li Z.,Wuhan University
Journal of Craniofacial Surgery | Year: 2014
Background: The appearance and dysfunction of deformities may cause psychologic disorders in patients. The aim of this study was to assess the psychologic health status of patients undergoing orthognathic surgery and its relationship with demographic characteristics, social activityof the individuals, and severity of maxillofacial deformity. Methods: As a tool for assessing the psychologic health status, the Symptom Checklist-90 (SCL-90) questionnaire was used on 318 patients undergoing orthognathic surgery at the Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, China from January 2006 to November 2012. t-Test was used to compare the psychologic health status between the 318 patients and 200 healthy volunteers. Variance analysis (analysis of variance) was applied for assessing the relationship between the psychologic health status and the variables of the study. Results: The SCL-90 total score of the patients undergoing orthognathic surgery was higher than that of the healthy volunteers (P < 0.05). Results of the t-test revealed statistically significant difference (P < 0.05) in the symptom dimensions of obsessive-compulsive, interpersonal sensitivity, depression, and paranoid ideation. An association between sex and the SCL-90 total score was observed (F = 11.293; P = 0.001 and P <0.05). The patients who had regular work presented better psychological health status than did the patients who had no regular work (F = 8.008; P = 0.005 and P < 0.05). The patients who received comfort from family and relatives presented better psychological health status than did the patients who did not receive such help (F = 10.064; P = 0.002 and P < 0.05). The patients who received economic help from family and relatives presented better psychological health status than did the patients who did not receive such help (F = 9.789; P = 0.002 and P < 0.05). An association was found between severity of deformity and psychologic health (F = 6.394; P = 0.002 and P < 0.05). Conclusions: Patients with jaw deformity have significant psychologic problems and their psychologic health is affected by demographic characteristics, social activity of individuals, and severity of maxillofacial deformity. Copyright © 2014 by Mutaz B. Habal, MD.
Chen H.,Huazhong University of Science and Technology |
Zheng C.,First Hospital of Wuhan |
Zhang X.,Huazhong University of Science and Technology |
Li J.,Wuhan University |
And 2 more authors.
Peptides | Year: 2011
Apelin, a newly identified bioactive adipokine, has been found to play important roles in multiple diseases, including diabetes, hypertension and cardiovascular diseases with unclear molecular mechanisms. The present study aimed to investigate the effects of apelin on endoplasmic reticulum (ER) stress in the pancreas of Akita mice, a well-established type 1 diabetic model. Apelin-13 (400 pmol/kg) was injected from tail vein for 10 weeks. The physiological characters of experimental animals were evaluated, pancreatic islet morphology and insulin content were assessed by immunohistochemistry, and ER stress markers in the pancreas were examined by Western blots. Our results indicate apelin treatment significantly ameliorates diabetes-induced reduction in pancreatic islet mass and insulin content. Further studies suggested apelin treatment alleviates ER stress by inhibiting the diabetes induced up-regulation of PERK and IRE1α and chaperones (GRP78, calnexin and Hsp70) levels in Akita mice. We also demonstrated that apelin treatment normalizes the diabetes induced alteration of AKT and ERK activations in the pancreas of Akita mice. Taken together, these results suggest a novel physiological role of apelin in alleviating ER stress in the pancreas of type 1 diabetes. © 2011 Elsevier Inc.
Zhou W.,Wuhan University |
Zhou W.,First Hospital of Wuhan |
Fu X.-Q.,Wuhan University |
Zhang L.-L.,Wuhan University |
And 9 more authors.
Cell Death and Disease | Year: 2013
The inherent resistance of tumors to DNA damage often limits the efficacy of chemotherapy. The aim of this work is to explore the potential mechanism for development of chemoresistance in gastric cancer. Our data revealed that AKT1 mRNA and protein expression were induced by doxorubicin (a chemotherapeutic agent); the doxorubicin-induced AKT1 expression and activation increased the binding of NF-kappaB on Notch1 DNA promoter and then promoted the Notch1 transcription and expression; enhanced expression of Notch1 further upregulated PTEN expression through CBF-1 binding to PTEN DNA promoter; and inhibition of AKT1 expression and activity sensitized the gastric cancer cell to doxorubicin treatment in cultured gastric cancer cell lines and xenograft nude mice gastric cancer model. Furthermore, our data demonstrated that both Notch1 and PTEN were absent or minimally expressed in gastric cancer tissue but abundant in paired normal gastric mucosa, and the expression of Notch1 correlated with that of PTEN. Together, these novel results suggested that a novel AKT1/NF-kappaB/ Notch1/PTEN axis has an important role in the development of chemoresistance in gastric cancer. Notch1 has an anti-cancer role in gastric cancer. © 2013 Macmillan Publishers Limited. All rights reserved.
PubMed | First Hospital of Wuhan, Massachusetts General Hospital and Huazhong University of Science and Technology
Type: | Journal: Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie | Year: 2016
The precise role of interleukin-1 beta (IL-1)-induced extracellular matrix degeneration in the pathogenesis of intervertebral disc degeneration (IDD) is currently unknown. Recent evidence has revealed that microRNAs (miRNAs) are associated with IDD, but their function in the extracellular matrix degradation of nucleus pulposus (NP) tissues is also poorly understood. The aim of this study was to evaluate the expression and functional role of miR-7 in IL-1-induced disc degeneration. The expression level of miR-7 was investigated in degenerative NP tissues and in IL-1-induced NP cells using quantitative reverse transcription-polymerase chain reaction amplification analysis. A dual-luciferase reporter assay was then utilized to determine whether growth differentiation factor 5 (GDF5) is a target of miR-7. Finally, mRNA and protein levels of known matrix components and of matrix degradation enzymes were determined to elucidate the function of miR-7 in IL-1-induced disc degeneration. In this study, we found that miR-7 is highly expressed in human degenerative NP tissues and in IL-1 stimulated NP cells compared to normal controls. We also determined that GDF5 was a target of miR-7. Functional analysis showed that the overexpression of miR-7 significantly enhanced the IL-1-induced extracellular matrix degeneration, whereas inhibition of miR-7 function by antagomiR-7 prevented NP cell detrimental catabolic changes in response to IL-1. Additionally, the prevention of IL-1-induced NP extracellular matrix degeneration by miR-7 silencing was attenuated by GDF5 siRNA. These findings suggest that miR-7 contributes to an impaired ECM in intervertebral discs through targeting GDF5 and miR-7 might therefore represent a novel therapeutic target for the prevention of IDD.
Liao Y.-H.,Huazhong University of Science and Technology |
Xia N.,Huazhong University of Science and Technology |
Zhou S.-F.,Huazhong University of Science and Technology |
Tang T.-T.,Huazhong University of Science and Technology |
And 12 more authors.
Journal of the American College of Cardiology | Year: 2012
Objectives: This study tested whether interleukin (IL)-17A is involved in the pathogenesis of mouse myocardial ischemia/reperfusion (I/R) injury and investigated the mechanisms. Background: Inflammatory processes play a major role in myocardial I/R injury. We recently identified IL-17A as an important cytokine in inflammatory cardiovascular diseases such as atherosclerosis and viral myocarditis. However, its role in myocardial I/R injury remains unknown. Methods: The involvement of IL-17A was assessed in functional assays in mouse myocardial I/R injury by neutralization/repletion or genetic deficiency of IL-17A, and its mechanism on cardiomyocyte apoptosis and neutrophil infiltration were further studied in vivo and in vitro. Results: Interleukin-17A was elevated after murine left coronary artery ligation and reperfusion. Intracellular cytokine staining revealed that γδT lymphocytes but not CD4+ helper T cells were a major source of IL-17A. AntiIL-17A monoclonal antibody treatment or IL-17A knockout markedly ameliorated I/R injury, as demonstrated by reduced infarct size, reduced cardiac troponin T levels, and improved cardiac function. This improvement was associated with a reduction in cardiomyocyte apoptosis and neutrophil infiltration. In contrast, repletion of exogenous IL-17A induced the opposite effect. In vitro study showed that IL-17A mediated cardiomyocyte apoptosis through regulating the Bax/Bcl-2 ratio, induced CXC chemokine-mediated neutrophil migration and promoted neutrophil-endothelial cell adherence through induction of endothelial cell E-selectin and inter-cellular adhesion molecule-1 expression. Conclusions: IL-17A mainly produced by γδT cells plays a pathogenic role in myocardial I/R injury by inducing cardiomyocyte apoptosis and neutrophil infiltration. © 2012 American College of Cardiology Foundation.
Yang C.,Zhongshan Hospital |
Hu D.-H.,Zhongshan Hospital |
Feng Y.,First Hospital of Wuhan
Molecular Medicine Reports | Year: 2015
Inhalation therapy using essential oils has been used to treat acute and chronic sinusitis and bronchitis. The aim of the present study was to determine the chemical composition of the essential oil of Artemisia capillaris, and evaluate the antibacterial effects of the essential oil and its main components, against common clinically relevant respiratory bacterial pathogens. Gas chromatography and gas chromatography-mass spectrometry revealed the presence of 25 chemical constituents, the main constituents being: α-pinene, β-pinene, limonene, 1,8-cineole, piperitone, β-caryophyllene and capillin. The antibacterial activities of the essential oil, and its major constituents, were evaluated against Streptococcus pyogenes, methicillin-resistant Staphylococcus aureus (MRSA), MRSA (clinical strain), methicillin-gentamicin resistant Staphylococcus aureus (MGRSA), Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae and Escherichia coli. The essential oil and its constituents exhibited a broad spectrum and variable degree of antibacterial activity against the various strains. The essential oil was observed to be much more potent, as compared with any of its major chemical constituents, exhibiting low minimum inhibitory and bacteriocidal concentration values against all of the bacterial strains. The essential oil was most active against S. pyogenes, MRSA (clinical strain), S. pneumoniae, K. pneumoniae, H. influenzae and E. coli. Piperitone and capillin were the most potent growth inhibitors, among the major chemical constituents. Furthermore, the essential oil of A. capillaris induced significant and dose-dependent morphological changes in the S. aureus bacterial strain, killing >90% of the bacteria when administered at a higher dose; as determined by scanning electron microscopy. In addition, the essential oil induced a significant leakage of potassium and phosphate ions from the S. aureus bacterial cultures. These results indicate that the antibacterial action of A. capillaris essential oil may be mediated through the leakage of these two important ions. In conclusion, A. capillaris essential oil exhibits potent antibacterial activity by inducing morphological changes and leakage of ions in S. aureus bacterial cultures.
Huang X.-L.,First Hospital of Wuhan |
Pan J.-H.,First Hospital of Wuhan |
Chen D.,First Hospital of Wuhan |
Chen J.,First Hospital of Wuhan |
And 2 more authors.
European Journal of Internal Medicine | Year: 2016
Background The current meta-analysis evaluated the outcomes of various lifestyle interventions, including diet modifications (DIET), physical activity (PA), and patient education (EDU) in reducing the risk of cardiovascular disease in patients with type 2 diabetes. Methods Randomized clinical trials comparing lifestyle intervention with "usual care" (control) in type 2 diabetes patients were hand-searched from medical databases by two independent reviewers using the terms "diabetes, cardiovascular risk, lifestyle, health education, dietary, exercise/physical activities, and behavior intervention". Results Of the 235 studies identified, 17 were chosen for the meta-analysis. The average age of patients ranged from 50-67.3 years. Results reveal no significant difference between the groups, with respect to BMI, while PA and DIET yielded a greater reduction in HbA1c. Significant reduction in both systolic and diastolic pressures in the DIET group, and diastolic pressure in the PA group, was observed. HDL-c in the DIET group was significantly higher than the control group, while no change in LDL-c levels, was seen in all three intervention subtypes. There was no difference between the EDU vs. the control group in terms of HbA1c, blood pressure or HDL-c and LDL-c. Conclusion DIET intervention showed an improvement in HbA1c, systolic/diastolic blood pressure and HDL-c, with an exception of LDL-c and BMI, suggesting that nutritional intervention had a significant impact on the quality of life by reducing the cardiovascular risk in type 2 diabetes patients. © 2015 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.
Zhu J.,First Hospital of Wuhan |
Cheng X.-K.,First Hospital of Wuhan
Zhonghua Shiyan Yanke Zazhi/Chinese Journal of Experimental Ophthalmology | Year: 2013
Background: Alkali burn-induced corneal neovascularization(CNV) usually leads to blindness. Recently, study determined that vascular endothelial growth factor(VEGF) and basic fibroblast growth factor(bFGF) were the main regulating factors inducing angiogenesis, and canstatin proteins can inhibit the growth of VEGF and bFGF and thereby inhibit CNV growth. Objective: The present study was to investigate the effect of recombinant canstatin protein on mouse CNV induced by alkali burn and its mechanism. Methods: CNV models were induced in the right eyes of 40 female BALB/c mice by sticking the 2.0 mm filtering paper with 1 mol/L NaOH at the central cornea for 10 seconds. The animals then were randomized into two groups. Recombinant canstatin protein drops(5 mg/L) was topically administered 4 times daily in the mice of the experimental group, and normal saline solution was used at the same way in the control group. Corneas of the mice were examined under the slit lamp to calculate the CNV area 1 day, 3, 7, 14 days after modeling. The mice were sacrificed at above time points and corneas were obtained. The expressions of VEGF protein and bFGF protein in cornea were detected by Western blot, and the results were analyzed by enhanced chemiluminescence(ECL). The use of the experimental animals complied with the Instructive Notions with Respect to Caring for Laboratory Animals by State Ministry of Science and Technology. Results: In 3, 7 and 14 days after establishment of models, the area of CNV was(1.98 ±0.31) mm2, (6.21 ±0.44) mm2 and (9.83 ±0.72) mm2 in the experimental group, and that in the control group was (2.92 ± 0.41) mm2, (8.04 ± 0.56) mm2 and (11.78 ± 0.84)mm2, showing significant reduce in the mice treated with recombinant canstatin protein (t3 d =4.332, P = 0.005; t7 d = 11.729, P = 0.000; t14 d = 14.562, P = 0.000). Western blot analysis showed that there was significant increase in the gray scale of VEGF protein 1 day, 3, 7, 14 days following alkali burn in the experimental group compared with the control group(t1 d = -3.980, P<0.001; t3 d = -10.020, P<0.001; t7 d = -4.355, P<0.001; t14 d = -8.156, P<0.001), and the gray scale of bFGF was significantly ascent at various time points in the the experimental in comparison with the control groups (t1 d = - 3.488, P < 0.001; t3 d = - 2.124, P = 0.013; t7 d = - 1.977, P = 0.028; t14 d= -4.542, P<0.001). Conclusions: Topical application of recombinant canstatin protein drops inhibits CNV growth induced by alkali burn by down-regulating the expressions of VEGF and bFGF proteins. Copyright © 2013 by the Chinese Medical Association.