ABSTRACT
Objective To assess the impact of physical training on physiological function of adult renal transplant recipients by meta-analysis and to provide theoretical guidance for clinical practice.Methods Randomized controlled trials of physical training for the treatment of renal transplant recipients until October 2017 were searched in the database of Cochrane library,PubMed,Embase,Web of Science,Wanfang Data and CNKI.Data extracted from the literatures were analyzed with RevMan software (version 5.3).Results A total of 10 studies in 10 manuscripts met the inclusion criteria,and 557 cases were included.Meta-analysis results were as follows.Compared with the control group (routine drug therapy),the level of peak exercise oxygen uptake (peak VO2) was significantly increased in physical training group (routine drug therapy and physical training) (MD=2.40,95％ CI 0.15-4.64,P=0.04).However,there was no statistically significant difference in the change of blood lipid,blood pressure,hemoglobin and serum creatinine between the two groups (all P ＞0.05).Conclusions Physical training can improve cardio respiratory fitness of renal transplant recipients in the early stage,but it has no obvious effect on blood pressure,blood lipid,hemoglobin and blood creatinine.
ABSTRACT
Objective To investigate the effect and the mechanism of epithelial-mesenchymal transition (EMT) in renal tubular cells induced by uric acid.Methods Normal rat kidney tubular cell line (NRK-52E) were exposed to different concentrations of uric acid (100,200,400,600,800 μmol/L UA) for 48 hours to induce EMT.Morphological changes of the NRK-52E cells were examined under an inverted phase contrast microscope.The protein expression of E-cadherin,α-SMA,p-Akt and Akt were detected by Western blotting.The distribution of E-cadherin and α-SMA were detected by immunofluorescence.NRK-52E cells were pretreated by different concentrations of LY294002(0,2.5,5,10,15 μmol/L),the inhibitor of PI3K/p-Akt signaling pathway,and then processed by uric acid (400 μmol/L) for 48 hours.Western blotting was used to detect the protein expression of p-Akt and Akt.NRK-52E cells were then divided into four groups:normal group (N),uric acid group (UA),LY294002 group (LY),uric acid with LY294002 group (UA + LY).The protein expression of E-cadherin and α-SMA were detected by Western blotting,the distribution of E-cadherin,α-SMA and p-Akt were detected by immunofluorescence.Results There was abundant cellular expression of E-cadherin in unstimulated renal tubular cells whereas its expression was significantly decreased in uric acidstimulated cells (P ＜ 0.05).In addition,uric acid induced de novo expression of α-SMA in contrast to almost negative staining in untreated cells (P ＜ 0.05).p-Akt were obviously increased in high uric acid group (P ＜ 0.05) and Akt changed not significantly (P ＞ 0.05).NRK-52E cells transformed into elongated fibroblast-like cells from cuboidal clustered epithelial cells.These indicated that uric acid has induced EMT and activated PI3K/p-Akt signaling pathway in NRK-52E cells.However,the above effects of uric acid were abolished when p-Akt was blocked by the PI3K inhibitor (10,15 μmol/L LY294002),indicated that LY294002 has reversed the trend of EMT.Conclusions High uric acid induces phenotypic transition of renal tubular cells probably via activating PI3K/Akt signaling pathway.