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Clinical observation of the reduced glutathione in the treatment of diabetic chronic kidney disease

Authors :
Hua-Guo Zhang
Miaomiao Xiang
Jianping Dai
Manhua Zuo
Jun Tang
Guo-Dan Yu
Hui Hu
Qing Long
Source :
Journal of Cellular Biochemistry. 120:8483-8491
Publication Year :
2018
Publisher :
Wiley, 2018.

Abstract

Background Diabetic chronic kidney disease (CKD) has become the main cause of death in diabetic patients, but its pathogenesis has not yet been clear. Objective To investigate the effects of reduced glutathione (GSH) on oxidative stress (OS), angiogenesis factors and lymphocyte subsets in diabetic CKD patients. Methods A total of 130 subjects were retrospectively studied. The subjects were divided into the control group (45 cases), treatment group (45 cases, treated with reduced GSH), and a healthy control group (40 cases). The levels of superoxide dismutase (SOD), advanced oxidation protein products (AOPP), malondialdehyde (MDA), endostatin (ES), and vascular endothelial growth factor (VEGF), and the percentages of lymphocyte subsets were detected. Results After treatment, the indexes of OS and angiogenesis and the percentage of CD3- CD19+ B cells were obviously decreased, and the percentages of T cell subsets and natural killer (NK) cell subsets were markedly increased in the treatment group compared with the control group. AOPP was positively correlated with angiogenesis indexes, MDA and CD3- CD19+ B cells, and negatively correlated with SOD and other lymphocyte subsets. SOD was inversely associated with angiogenesis indexes and MDA, and positively associated with lymphocyte subsets. Moreover, MDA had a positive correlation with angiogenesis indexes, B and T cell subsets, and a negative correlation with NK cell subsets. AOPP, MDA, SOD, VEGF, CD3+ T cells, CD3+ CD8+ T cells, CD3- CDl6+ CD56+ NK cells, and CD3- CDl6+ CD56+ NK T cells were the risk factors of diabetic CKD. Conclusion GSH could inhibit OS and abnormal angiogenesis, and improve cellular immune response in CKD patients.

Details

ISSN :
10974644 and 07302312
Volume :
120
Database :
OpenAIRE
Journal :
Journal of Cellular Biochemistry
Accession number :
edsair.doi.dedup.....b45ab183127abac0ae045633f22ec015