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1.
Front Endocrinol (Lausanne) ; 15: 1356131, 2024.
Article in English | MEDLINE | ID: mdl-38711978

ABSTRACT

Objective: Diabetic nephropathy (DN) is a major microvascular complication of diabetes and the leading cause of end-stage renal disease. Early detection and prevention of DN are important. Retinol-binding protein 4 (RBP4) has been considered as a single diagnostic marker for the detection of renal impairment. However, the results have been inconsistent. The present meta-analysis aimed to determine the diagnostic potential of RBP4 in patients in type 2 diabetes mellitus (T2DM) with DN. Methods: We searched PubMed, Web of Science, Embase, Wanfang and CNKI databases from inception until January 2024. The meta-analysis was performed by Stata version 15.0, and sensitivity, specificity, positive and negative likelihood ratios (PLR and NLR), diagnostic odds ratio (DOR) and area under the curve (AUC) were pooled. The Quality Assessment of Diagnostic Accuracy Studies-2 tool was utilized to assess the quality of each included study. In addition, heterogeneity and publication bias were evaluated. Results: Twenty-nine studies were included in the meta-analysis. The pooled sensitivity and specificity were 0.76 [95% confidence interval (CI), 0.71-0.80] and 0.81 (95% CI, 0.76-0.85), respectively. The results showed a pooled PLR of 4.06 (95% CI, 3.16-5.21), NLR of 0.29 (95% CI, 0.24-0.36) and DOR of 13.76 (95% CI, 9.29-20.37). The area under the summarized receiver operating characteristic curve was given a value of 0.85 (95% CI, 0.82-0.88). No obvious publication bias existed in the Deeks' funnel plot asymmetry test. Conclusion: Our findings suggest that RBP4 has a promising diagnostic value with good sensitivity and specificity for patients with T2DM with DN.


Subject(s)
Diabetic Nephropathies , Retinol-Binding Proteins, Plasma , Humans , Diabetic Nephropathies/diagnosis , Retinol-Binding Proteins, Plasma/metabolism , Retinol-Binding Proteins, Plasma/analysis , Diabetes Mellitus, Type 2/complications , Diabetes Mellitus, Type 2/diagnosis , Biomarkers/blood , Sensitivity and Specificity
2.
BMC Complement Altern Med ; 19(1): 193, 2019 Jul 30.
Article in English | MEDLINE | ID: mdl-31362740

ABSTRACT

BACKGROUND: Wenshen Jianpi recipe (WSJPR), a blended traditional Chinese medicine, is considered to have the possible beneficial effect on the progression of diabetic nephropathy (DN). This present study was designed to elucidate this protective activity in a rat model with streptozotocin (STZ)-induced DN and to explore the possible underlying mechanism. METHODS: Adult Sprague Dawley (SD) rats were induced to develop DN through intraperitoneal injection of STZ (60 mg/kg). Animals were orally administered saline, WSJPR at 7.5, 15, 30 g/kg, and valsartan (25 mg/kg) daily for 8 weeks. Blood and 24-h urine samples of each rat were collected for biochemical examination at 2-week intervals. Microcirculatory blood flow in the renal cortex and hemorheology index were also measured. At the end of 8 weeks, all rats were sacrificed to obtain the kidney tissues for histological examination and reverse transcription polymerase chain reaction (RT-PCR) was used to analyze the transcriptional levels of nephrin and podocin genes. RESULTS: WSJPR could improve serum total protein (TP) and albumin (ALB), reduce the excretion rates of urine-TP (U-TP), urine-ALB (U-ALB) and urine urea nitrogen (UUN) (P < 0.05), although it did not significantly alter the hyperglycemia. In addition, treatment with WSJPR could strongly reduce blood flow, erythrocyte aggregation index, and ameliorate microcirculation. In histological measurement, WSJPR-treated rats showed a significant amelioration in glomerular hypertrophy and mesangial expansion. By RT-PCR, we found WSJPR up-regulated the nephrin and podocin expression at mRNA levels. CONCLUSION: This study suggested that WSJPR could effectively relieve renal damage and improve renal function of DN rats by ameliorating metabolism disorder and increasing the gene expression of nephrin and podocin, which might be a useful approach for the treatment of DN.


Subject(s)
Diabetic Nephropathies/drug therapy , Drugs, Chinese Herbal/administration & dosage , Proteinuria/drug therapy , Animals , Diabetic Nephropathies/genetics , Diabetic Nephropathies/metabolism , Disease Models, Animal , Drugs, Chinese Herbal/chemistry , Humans , Intracellular Signaling Peptides and Proteins/genetics , Intracellular Signaling Peptides and Proteins/metabolism , Kidney/drug effects , Kidney/injuries , Kidney/metabolism , Male , Medicine, Chinese Traditional , Membrane Proteins/genetics , Membrane Proteins/metabolism , Proteinuria/genetics , Proteinuria/metabolism , Rats , Rats, Sprague-Dawley
3.
Artif Cells Nanomed Biotechnol ; 47(1): 2379-2388, 2019 Dec.
Article in English | MEDLINE | ID: mdl-31184222

ABSTRACT

Diabetes mellitus (DM) is a metabolic disorder that seriously harms human health. Notoginsenoside R1 (NGR1) can be used in various diseases. We explored consequents of NGR1 on tumour necrosis factor (TNF)-α-stimulated Min6 and rat primary islets ß cells. The results were that TNF-α significantly cut down cell activity, raised cell apoptosis and iNOS expression and decreased insulin secretion in Min6 and rat primary islets ß cells. NGR1 alleviated TNF-α-treated cell dysfunctions. In addition, miR-29a was positively regulated by NGR1 in TNF-α-treated Min6 and rat primary islets ß cells. miR-29a knockdown damaged protection roles of NGR1 through cutting down cell activity and insulin secretion, raising apoptosis and iNOS in TNF-α-treated Min6 and rat primary islets ß cells. The phosphorylation of Wnt3a, ß-catenin and the rate of p/t-AKT/PI3K was all increased, while p/t-GSK3ß was decreased by the administration with NGR1. In conclusion, NGR1 alleviated TNF-α-stimulated Min6 and rat primary islets ß cells apoptosis and worn roles via positively regulating miR-29a. This process might be through actuation of Wnt/ß-catenin and PI3K/AKT/GSK3ß signal ways.


Subject(s)
Apoptosis/drug effects , Ginsenosides/pharmacology , Insulin-Secreting Cells/cytology , Insulin-Secreting Cells/drug effects , MicroRNAs/genetics , Tumor Necrosis Factor-alpha/pharmacology , Up-Regulation/drug effects , Animals , Cell Line, Tumor , Glycogen Synthase Kinase 3 beta/metabolism , Insulin-Secreting Cells/metabolism , Mice , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Rats , Wnt Signaling Pathway/drug effects
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