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.