Proteomics analysis of lung tissue reveals protein makers for the lung injury of adjuvant arthritis rats.

Lung injury is one of the common extra­articular lesions in rheumatoid arthritis (RA). Due to its insidious onset and no obvious clinical symptoms, it can be easily dismissed in the early stage of diagnosis, which is one of the reasons that leads to a decline of the quality of life and subsequent death of patients with RA. However, its pathogenesis is still unclear and there is a lack of effective therapeutic targets. In the present study, tandem mass tag­labeled proteomics was used to research the lung tissue proteins in RA model (adjuvant arthritis, AA) rats that had secondary lung injury. The aim of the present study was to identify the differentially expressed proteins related to RA­lung injury, determine their potential role in the pathogenesis of RA­lung injury and provide potential targets for clinical treatment. Lung tissue samples were collected from AA­lung injury and normal rats. The differentially expressed proteins (DEPs) were identified by tandem mass spectrometry. Bioinformatic analysis was used to assess the biological processes and signaling pathways associated with these DEPs. A total of 310 DEPs were found, of which 244 were upregulated and 66 were downregulated. KEGG anlysis showed that 'fatty acid degradation', 'fatty acid metabolism', 'fatty acid elongation', 'complement and coagulation cascades', 'peroxisome proliferator­activated receptor signaling pathway' and 'hypoxia­inducible factor signaling pathway' were significantly upregulated in the lung tissues of AA­lung injury. Immunofluorescence staining confirmed the increased expression of clusterin, serine protease inhibitors and complement 1qc in lung tissue of rats with AA lung injury. In the present study, the results revealed the significance of certain DEPs (for example, C9, C1qc and Clu) in the occurrence and development of RA­lung injury and provided support through experiments to identify potential biomarkers for the early diagnosis and prevention of RA­lung injury.

Roles of Gut Microbiota in Pathogenesis of Alzheimer's Disease and Therapeutic Effects of Chinese Medicine.

Alzheimer's disease (AD) is the most common neurodegenerative disease characterized by progressive cognitive impairment. The pathogenesis of AD is complex, and its susceptibility and development process are affected by age, genetic and epigenetic factors. Recent studies confirmed that gut microbiota (GM) might contribute to AD through a variety of pathways including hypothalamic pituitary adrenal axis and inflflammatory and immune processes. CM formula, herbs, and monomer enjoy unique advantages to treat and prevent AD. Hence, the purpose of this review is to outline the roles of GM and its core metabolites in the pathogenesis of AD. Research progress of CMs regarding the mechanisms of how they regulate GM to improve cognitive impairment of AD is also reviewed. The authors tried to explore new therapeutic strategies to AD based on the regulation of GM using CM.

Identification of Candidate Genes Related to Synovial Macrophages in Rheumatoid Arthritis by Bioinformatics Analysis.

OBJECTIVE: Rheumatoid arthritis (RA) is one of the most prevalent inflammatory arthritis worldwide. However, the genes and pathways associated with macrophages from synovial fluids in RA patients still remain unclear. This study aims to screen and verify differentially expressed genes (DEGs) related to identifying candidate genes related to synovial macrophages in rheumatoid arthritis by bioinformatics analysis. METHODS: We searched the Gene Expression Omnibus (GEO) database, and GSE97779 and GSE10500 with synovial macrophages expression profiling from multiple RA microarray dataset were selected to conduct a systematic analysis. GSE97779 included nine macrophage samples from synovial fluids of RA patients and five macrophage samples from primary human blood of HC. GSE10500 included five macrophage samples from synovial fluids of RA patients and three macrophage samples from primary human blood of HC. Functional annotation of DEGs was performed, including Gene Ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Protein-protein interaction (PPI) network of DEGs was established using the STRING database. CytoHubba was used to identify hub genes. MCODE was used to determine gene clusters in the interactive network. RESULTS: There were 2638 DEGs (1425 upregulated genes and 1213 downregulated ones) and 889 DEGs (438 upregulated genes and 451 downregulated ones) selected from GSE97779 and GSE10500, respectively. Venn diagrams showed that 173 genes were upregulated and 106 downregulated in both two datasets. The top 10 hub genes, including FN1, VEGFA, HGF, SERPINA1, MMP9, PPBP, CD44, FPR2, IGF1, and ITGAM, were identified using the PPI network. CONCLUSION: This study provides new insights for the potential biomarkers and the relevant molecular mechanisms in RA patients. Our findings suggest that the 10 candidate genes might be used in diagnosis, prognosis, and therapy of RA in the future. However, further studies are required to confirm the expression of these genes in synovial macrophages in RA and control specimen.

[Effects of electroacupuncture on skeletal muscle and blood glucose in rats with diabetic amyotrophy].

OBJECTIVE: To explore the effects of electroacupuncture (EA) on skeletal muscle and blood glucose in rats with diabetic amyotrophy. METHODS: Among 40 SD rats, 10 rats were randomly selected into the control group and received no treatment. The remaining 30 rats were treated with intraperitoneal injection of streptozotocin (STZ, 60 mg/kg) to establish diabetes mellitus (DM) model, and then the rats were treated with vascular ligation at right posterior limb to establish amyotrophy model. The rats with diabetic amyotrophy were randomly divided into a model group and an EA group, 10 rats in each group (10 rats were excluded due to unsuccessful model establishment and death). The rats in the EA group was treated with EA at right-side "Yishu (EX-B 3)" "Shenshu (BL 23)" "Zusanli (ST 36)" and "Sanyinjiao (SP 6)", disperse-dense wave, 2 Hz/ 15 Hz, 20 minutes each time, once a day for 3 weeks. Before and after EA treatment, the blood sample was collected from inner canthus and the "glucose oxidase-peroxidase" method was used to detect fasting blood glucose level; ELISA method was used to detect insulin content. At the end of the treatment, HE staining method was used to observe the morphology of ischemic skeletal muscle in the right hindlimb; the real-time PCR method was used to detect the mRNA expression of muscle atrophy F-box (MAFbx), muscle ring finger-1 (MuRF1) and forkhead box O3a (FOXO3a) in the ischemic skeletal muscle tissue of right hindlimb. RESULTS: Before the treatment, the body mass in the model group and EA group was lower than that in the control group (P<0.01); after the treatment, the body mass in the control group was increased, while the body mass in the model group and EA group was decreased (P<0.01). Compared with the control group, the fasting blood glucose was significantly increased and insulin content was significantly decreased in the model group (P<0.01); compared with the model group, the fasting blood glucose was significantly decreased and the insulin content was significantly increased in the EA group after treatment (P<0.01). The muscle fibers of the model group were obviously broken, the number of the nuclei decreased, and the nuclei shrinked or even dissolved; the morphology of the muscle tissue of the EA group after intervention was improved compared with the model group. Compared with the control group, the cross-sectional area of ischemic skeletal muscle cells in the right hindlimb in the model group was decreased (P<0.01); compared with the model group, the cross-sectional area of ischemic skeletal muscle cells in the right hindlimb was increased in EA group (P<0.05). Compared with the control group, the levels of MAFbx, MuRF1 and FOXO3a mRNA in the right hindlimb ischemic skeletal muscle in the model group were increased significantly (P<0.01, P<0.05); compared with the model group, the levels of MAFbx, MuRF1 and FOXO3a mRNA in the EA group were decreased significantly (P<0.05, P<0.01). CONCLUSION: EA may play a role in the treatment of diabetic amyotrophy by inducing FOXO3a to reduce the transcription of MAFbx and MuRF1.