The First Affiliated Hospital of Nanchang UniversityJiangxi

Nanchang, China

The First Affiliated Hospital of Nanchang UniversityJiangxi

Nanchang, China
SEARCH FILTERS
Time filter
Source Type

Zhu Y.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Cheng M.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Yang Z.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Zeng C.-Y.,The First Affiliated Hospital of Nanchang UniversityJiangxi | And 6 more authors.
Drug Design, Development and Therapy | Year: 2014

Mesenchymal stem cells (MSCs) have been recognized as promising delivery vehicles for gene therapy of tumors. Gastric cancer is the third leading cause of worldwide cancer mortality, and novel treatment modalities are urgently needed. NK4 is an antagonist of hepatocyte growth factor receptors (Met) which are often aberrantly activated in gastric cancer and thus represent a useful candidate for targeted therapies. This study investigated MSC-delivered NK4 gene therapy in nude mice bearing gastric cancer xenografts. MSCs were transduced with lentiviral vectors carrying NK4 complementary DNA or enhanced green fluorescent protein (GFP). Such transduction did not change the phenotype of MSCs. Gastric cancer xenografts were established in BALB/C nude mice, and the mice were treated with phosphate-buffered saline (PBS), MSCs-GFP, Lenti-NK4, or MSCs-NK4. The tropism of MSCs toward gastric cancer cells was determined by an in vitro migration assay using MKN45 cells, GES-1 cells and human fibroblasts and their presence in tumor xenografts. Tumor growth, tumor cell apoptosis and intratumoral microvessel density of tumor tissue were measured in nude mice bearing gastric cancer xenografts treated with PBS, MSCs-GFP, Lenti-NK4, or MSCs-NK4 via tail vein injection. The results showed that MSCs migrated preferably to gastric cancer cells in vitro. Systemic MSCs-NK4 injection significantly suppressed the growth of gastric cancer xenografts. MSCs-NK4 migrated and accumulated in tumor tissues after systemic injection. The microvessel density of tumor xenografts was decreased, and tumor cellular apoptosis was significantly induced in the mice treated with MSCs-NK4 compared to control mice. These findings demonstrate that MSC-based NK4 gene therapy can obviously inhibit the growth of gastric cancer xenografts, and MSCs are a better vehicle for NK4 gene therapy than lentiviral vectors. Further studies are warranted to explore the efficacy and safety of the MSC-based NK4 gene therapy in animals and cancer patients. © 2014 Zhu et al.


Dong X.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Liu D.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Huang F.,The First Affiliated Hospital of Nanchang UniversityJiangxi
Chinese Journal of Rehabilitation Medicine | Year: 2017

Objective: To explore the wake-promoting effects and possible mechanisms of vagus nerve stimulation (VNS) in traumatic brain injury induce-coma rats. Method: SD rats were randomly divided into three groups: control, sham-stimulated (TBI) and stimulated (TBI+ VNS) group. ELISA, Western blot and immunohistochemistry technique were used to detect the expression of Orexin-A and OX1R level in prefrontal cortex (PFC) and hypothalamus area. Result: Twenty of 30 rats exhibited righting reflex in stimulated group, and 8 of 30 rats had the same responses in TBI groups. Orexin-A and OX1R levels in stimulated groups were higher than TBI groups both in PFC and hypothalamus area (P<0.05). Conclusion: VNS could raise consciousness in TBI induced coma rats, and the potential mechanism may be upregulating the expression of Orexin-A and OX1R in PFC and hypothalamus area. Therefore, VNS may be used as a wake-promoting method for patient after brain injury. © 2017, Editorial Board of Chinese Journal of Rehabilitation Medicine. All right reserved.


Liu S.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Zhang J.,Huazhong University of Science and Technology | Yu B.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Huang L.,The First Affiliated Hospital of Nanchang UniversityJiangxi | And 4 more authors.
American Journal of Translational Research | Year: 2016

Background: The aim of this study was to explore the role of autophagy in the cold I/R injury following lung transplantation. Methods: The rat orthotopic lung transplantation model was established to perform the level of autophagy in the cold I/R injury in this study. The pretreatment of inhibitor (3-Methyladenine [3-MA]) and activator (rapamycin [RAPA])of autophagy were performed to assess the role of autophagy in the cold I/R injury following lung transplantation in rats. Results: After lung transplantation, the autophagy, lung cell apoptosis and lung injury were aggravated and peaked at 6 h following the transplantation. The inhibition of autophagy by 3-MA induced downregulated of autophagy, decreased cell apoptosis. Meanwhile, the lung injury, which was indicated by calculating the peak inspiratory pressure (PIP), pulmonary vein blood gas analysis (PO2) and ratio of wet to dry in lung (W/D), was ameliorated after treatment with 3-MA. The activation of autophagy by RAPA causing the upregulated of autophagy and apoptosis of lung cells, and enhanced the lung injury. Conclusion: All the results suggested that the autophagy was involved in the cold I/R injury in lung transplantation model, and played a potential role on the regulation of I/R injury after lung transplantation. © 2016, E-Century Publishing Corporation. All rights reserved.


Tang J.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Tang S.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Liu J.,The First Affiliated Hospital of Nanchang UniversityJiangxi | Wu Q.,The First Affiliated Hospital of Nanchang UniversityJiangxi | And 2 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Background/Aim: Several reports have investigated the role of exonuclease 1 (EXO1) rs1047840 in lung cancer risk in different ethnic populations. Nevertheless, the results have been controversial. We aimed to assess the possible association between EXO1 rs1047840 and risk of lung cancer in a meta-analysis. Methods: Human hospital- or population-based studies released before December 16, 2013 were identified by systematic search of the PubMed and Embase databases. Data were extracted in duplicate from each study. An OR and 95% CI (odds ratio and 95% confidence interval) was calculated to evaluate the effects of EXO1 rs1047840 on lung carcinogenesis. Results: A total of 1,114 lung cancer patients and 1,166 well-matched controls were analyzed in this study. The fixed-effects meta-analysis revealed that carriage of a single A allele, compared to the carriage of single G allele, was associated with 1.18 times increased risk of lung cancer (A vs. G: OR =1.18; 95% CI: 1.03-1.35; PHeterogeneity, 0.121). Conclusion: This first meta-analysis demonstrates that the A allele of EXO1 rs1047840 may confer modulating effects on the risk of lung cancer and could be used as a marker for early detection and primary prevention. © 2015 E-Century Publishing Corporation. All rights reserved.

Loading The First Affiliated Hospital of Nanchang UniversityJiangxi collaborators
Loading The First Affiliated Hospital of Nanchang UniversityJiangxi collaborators