Background: Chinese herbal medicine (CHM) has the advantage of being safe and effective and has been widely used in clinical practice for the treatment of type 2 diabetes mellitus (T2DM) with hyperuricemia (HUA), but its overall efficacy and safety remain unclear. This study aimed to evaluate the efficacy and safety of CHM for the treatment of T2DM with HUA based on randomized controlled trials (RCTs) to provide clinical evidence.Methods: The protocol evaluated in this study is registered with PROSPERO (CRD42022351519). As of November 2022, eight databases were searched, and RCTs of CHM for the treatment of T2DM with HUA were included. Outcome indicators observed included fasting blood glucose (FBG), 2-h postprandial glucose (2hPG), glycated hemoglobin (HbA1c), uric acid (UA), triglycerides (TG), total cholesterol (TC), overall effectiveness, and adverse events. Utilizing Review Manager 5.4, Stata V14.0, and GRADEpro, the included studies were evaluated, and the quality of the evidence was determined.Results: 18 RCTs covering 1,311 patients were included in this study. The results of the study demonstrated that the combination of CHM and western medicine (WM) was more effective in treating patients with T2DM with HUA than WM alone, with significant improvements in FBG (weighted mean differences (WMD) = −0.60.95% confidence interval (CI) [−0.81, −0.40], p < 0.00001), 2hPG (WMD = −1.12.95% CI [−1.64, −0.60], p < 0.0001), HbA1c (WMD = −0.80.95% CI [−1.04, −0.56], p < 0.00001), UA (WMD = −53.47.95% CI [−67.45, −39.48], p < 0.00001), TG (WMD = −0.56.95% CI [−0.74, −0.38], p < 0.00001), TC (WMD = −0.49.95% CI [−0.65, −0.33], p < 0.00001), and overall effective rate (risk ratio (RR) = 1.29.95%CI [1.13, 1.48], p = 0.0002). The quality of evidence for all outcomes was low.Conclusion: Compared with WM alone, the combination of CHM and WM was more effective in treating patients with T2DM with HUA, with significant improvements in glucose metabolism, uric acid, and lipids. However, further evaluation by high−quality RCT results is needed due to the low quality and high heterogeneity of the evidence.Systematic Review Registration: [https://systematicreview.gov/], identifier [CRD42022351519].
Idiopathic pulmonary fibrosis (IPF) is a chronic progressive fibrotic disease with unclear etiology and no effective treatment. This study aims to reveal the pathogenetic mechanism networks of multiple targets and pathways of IPF. Extract and metabolites of Astragalus membranaceus (AM) and Radix paeoniae rubra (RPR), two well-known traditional Chinese medicine have been proven to be effective in IPF. However, the underlying mechanisms of AM and RPR in remain unclear. Based on network pharmacology analysis, differentially expressed genes (DEGs) of IPF were obtained from the GEO database. Targets of Astragalus membranaceus and Radix paeoniae rubra were identified using TCM Systems Pharmacology Database and Analysis Platform and SwissTargetPrediction. Subsequently, a protein-protein interaction (PPI) network was built and analyzed using the STRING database and Cytoscape software. Gene Ontology (GO) enrichment analysis and Kyoto Encyclopedia of Gene and Genomes (KEGG) analysis were performed using Metascape. Further, a component-target-pathway network and a Sankey diagram were used to obtain main active components and molecular docking was performed between the key active components and proteins encoded by key targets. Finally, in vivo studies were carried out based on network pharmacology. 117 common targets between DEGs of IPF and targets of drugs were screened out and included in the PPI network, in which AKT1, MAPK3, HSP90AA1, VEGFA, CASP3, JUN, HIF1A, CCND1,PTSG2 and MDM2 were predicted as the key targets. 117 targets were enriched in PI3K-AKT pathway, HIF-1 signaling pathway, apoptosis and MicroRNAs in cancer. Astragaloside III, (R)-Isomucronulatol, Astragaloside I, Paeoniflorin and β-sitosterol were selected as the main active components. The docking scores ranged from − 4.7 kcal/mol to -10.7 kcal/mol, showing a good binding affinity between main active compounds and key targets. In vivo studies indicated that AM and RPR ameliorated pathological lung fibrotic damage caused by bleomycin and reduced mRNA level of AKT1, HSP90AA1, CASP3, MAPK3 and VEGFA. In conclusion, this study identified AM and RPR as potential therapeutic agents for IPF via regulating AKT1, HSP90AA1, CASP3, MAPK3 and VEGFA.
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