Aim. The renal protective mechanisms of Shenyuan particle (SYP) in the treatment of diabetic kidney disease (DKD) were investigated, focusing on the main targets and pathways. Materials and Methods. In this study, the potential targets of compounds identified in SYP were predicted by Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP), and a “herb-compound-target” network was constructed via Cytoscape. Next, the Gene Ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analyses were dissected using R language. A protein-protein interaction network was fabricated using STRING to obtain the main target information. In addition, db/db mice were used as the DKD models to explore the renal protective effects of SYP. Transmission electron microscopy, western blot, pathological staining, TUNEL staining, and biochemical methods were used to identify the apoptotic pathways and establish the primary mechanism of SYP. Results. Network pharmacology analysis revealed 67 potential targets based on the analysis of different databases. The targets of SYP were primarily associated with apoptosis. The network hub genes included caspase 3, caspase 7, caspase 8, caspase 9, Bax, and Bcl-2. In vivo, SYP materially improved renal function and inhibited apoptosis in the db/db mouse kidneys by improving the mitochondrial health. In addition, our results showed that SYP significantly decreased the expression of Bax, caspase 3, and Cyto-c and increased the expression of Bcl-2. Conclusions. Network pharmacology analysis and experimental results suggest that SYP ameliorates DKD mediated via multiple components, targets, and pathways. Our study further demonstrates that SYP inhibits apoptosis in the kidneys of db/db mice by improving the mitochondrial health and thereby alleviating renal damage.

Background Idiopathic pulmonary fibrosis (IPF) is a fatal respiratory disease without effective treatments. Mitochondrial dysfunction weakens the ability of mesenchymal stem cells (MSCs) to repair the distal lung epithelium, which is a probable pathogenesis of IPF. In previous research, we found that cinnamaldehyde (CA) can maintain the mitochondrial morphology of MSCs. Methods This present study evaluated the effect and mechanism of CA on murine lung MSCs using the hydrogen peroxide model. Antioxidant effects and mitochondrial function were determined using flow cytometry. The mRNA levels of mitochondrial dynamics and the expressions of autophagy-related proteins were also detected. Results CA can increase the levels of SOD, MMP and ATP, decrease the rate of ROS and apoptosis, and restore the mitochondrial structure. CA can also improve the mRNA expression of MFN1, MFN2, FIS1, DRP1, OPA1, and PGC-1α, increase the expression of LC3 II and p62 and promote the PINK1/Parkin signaling pathway. Our results demonstrated that CA can control mitochondrial quality and avoid apoptosis, which may be associated with the regulation of the PINK1/Parkin signaling pathway.

Background Idiopathic pulmonary fibrosis (IPF) is the most common and serious type of idiopathic interstitial pneumonia, characterized by chronic, progressive, and low survival rates, while unknown disease etiology. Until recently, patients with idiopathic pulmonary fibrosis have a poor prognosis, high mortality, and limited treatment options, due to the lack of effective early diagnostic and prognostic tools. Therefore, we aimed to identify biomarkers for idiopathic pulmonary fibrosis based on multiple machine-learning approaches and to evaluate the role of immune infiltration in the disease. Method Next, the differentially expressed genes (DEGs) with the threshold of FDR < 0.05 and |log2 foldchange (FC)| > 0.585 were analyzed via R package “DESeq2” and GO enrichment and KEGG pathways were run in R software. Then, least absolute shrinkage and selection operator (LASSO) logistic regression, support vector machine-recursive feature elimination (SVM-RFE) and random forest (RF) algorithms were combined to screen the key potential biomarkers of idiopathic pulmonary fibrosis. The diagnostic performance of these biomarkers was evaluated through receiver operating characteristic (ROC) curves. Moreover, the CIBERSORT algorithm was employed to assess the infiltration of immune cells and the relationship between the infiltrating immune cells and the diagnostic biomarkers. Finally, we sought to understand the role of the diagnostic biomarker (SLAIN1) in idiopathic pulmonary fibrosis pathogenesis using a mouse model and cellular model. Results A total of 3658 differentially expressed genes of idiopathic pulmonary fibrosis were identified, including 2359 upregulated genes and 1299 downregulated genes. FHL2, HPCAL1, RNF182, and SLAIN1 were identified as diagnostic biomarkers of idiopathic pulmonary fibrosis using LASSO logistic regression, RF, and SVM-RFE algorithms. The ROC curves confirmed the predictive accuracy of these diagnostic biomarkers both in the training set and test set. Immune cell infiltration analysis suggested that patients with idiopathic pulmonary fibrosis had a higher level of B cells memory, Plasma cells, T cells CD8, T cells follicular helper, T cells regulatory (Tregs), Macrophages M0, and Mast cells resting compared with the control group. Correlation analysis demonstrated that FHL2 was significantly associated with the infiltrating immune cells. qPCR and western blotting analysis suggested that SLAIN1 might be a signature for the diagnosis of idiopathic pulmonary fibrosis. Conclusion In this study, we developed a diagnostic model to identify four diagnostic biomarkers (FHL2, HPCAL1,RNF182 and SLAIN1) and validated the role of SLAIN1 in the pathogenesis of idiopathic pulmonary fibrosis, which may be great significance in guiding the prognosis and treatment of idiopathic pulmonary fibrosis.

Background: The anti-inflammatory effect of vitamin D in patients with chronic kidney disease (CKD) remains controversial. This study aimed to conduct a meta-analysis of randomized controlled trials to assess the antiinflammatory effects of vitamin D in patients with CKD. Methods: We searched Embase, Science Citation Index, Medline, Cochrane Central Register of Controlled Trials, and Clinical Trial Registries for randomized controlled trials that comparing vitamin D with control groups for inflammatory markers in patients with CKD. Subgroup analysis was performed based on treatment duration (short-term treatment, long-term treatment), type of patients (predialysis CKD, dialysis, kidney transplant), 25(OH)D levels (25 (OH)D deficiency or normal 25(OH)D), and methods of C-reactive protein (CRP) test (standard CRP test or high-sensitivity CRP [hs-CRP] test).Results: Eighteen trials with 1834 patients were included in the present study. There were no significant differences between the vitamin D group and control group for CRP (WMD, À0.3 mg/L; 95% CI, À0.81 to 0.22, p = 0.26, I 2 = 62%), interleukin-6 (IL-6) (WMD, À1.07 pg/ml; 95% CI, À2.44 to 0.30, p = 0.12, I 2 = 52%), and tumor necrosis factor-α (TNF-α) (WMD, À0.00 pg/ml; 95% CI, À0.36 to 0.35, p = 0.99, I 2 = 0%) in patients with CKD. Subgroup analysis showed vitamin D can improve hs-CRP, but not CRP. The rest of subgroups showed that no significant differences were observed between the vitamin D group and control group based on 25(OH)D levels, treatment duration, and predialysis CKD or dialysis patients. Conclusion: This meta-analysis demonstrates that vitamin D supplementation does not have anti-inflammatory effects in CKD patients. Well-designed randomized controlled trials with large samples are required to confirm this conclusion. It is still needed to find an effective treatment for inflammatory state in CKD.

Introduction In this study, we will combine the traditional Baduanjin with Yijin Jing and Wuqinxi to create an optimized Baduanjin exercise program with three different forms (vertical, sitting, and horizontal) to adapt to idiopathic pulmonary fibrosis (IPF) patients in vairous stages of the disease. The purpose of this study is to explore and compare the therapeutic effects of this multi-form Baduanjin, traditional Baduanjin, and resistance training on lung function and limb motor function in IPF patients. The goal of this study is to prove a novel optimal exercise prescription strategy of Baduanjin exercise for improving and protecting lung function in IPF patients. Methods/design A single-blind and randomized controlled trial is used to conduct this study, while the randomization list will be generated using a computerized random number generator and opaque sealed envelopes with group allocation will be prepared. It will be strictly followed to blind the outcome assessors. and until the experiment’s conclusion, participants won’t know which group they are enrolled in. Patients between the ages of 35 and 80 who have stable diseases and have not regularly practiced Baduanjin exercise in the past will be included. They are divvied up into the following five groups at random: (1) The conventional care group (control group, CG), (2) The traditional Baduanjin exercise group (TG), (3) The modified Baduanjin exercise group (IG), (4) The resistance exercise group (RG) (5) The modified Baduanjin exercise combined with resistance exercise group (IRG). Those CG participants only received the usual treatment, while TC, IG, and RG participants exercised 1 h twice a day for 3 months. MRG participants will have a 3-month intervention with 1 h of Modified Baduanjin Exercise and 1 H of Resistance Training for each day. Every week, all groups underwent will supervis one-day training, with the exception of the control group. The Pulmonary Function Testing (PFT), HRCT, and 6MWT are the main outcome variables. The St. George Respiratory Questionnaire and mMRC are used as secondary outcome measures. Discussion This study may produce a new Baduanjin exercise prescription that is user-friendly, simple to execute, more targeted, and adaptable. Because it consists of three forms, including vertical, sitting, and horizontal, it is more adaptable to the various disease stages and actual situations of IPF patients and may compensate for the shortcomings of conventional pulmonary rehabilitation and traditional Baduanjin. Trial registration Chinese Clinical Trial Registry, ChiCTR2200055559. Registered on 12 January 2022.