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Effect of SEW, FIR on general observation of lung tissue in each group. Black arrow stands for ecchymosis while red arrow stands for edema.
Source publication
Objective:
To explore the protective effect of special electromagnetic field treated water (SEW) and far infrared rays (IFR) on endotoxin (lipopolysaccharide, LPS) induced ARDS rats and the effect on inflammatory factors.
Methods:
40 healthy male SD rats were randomly divided into 4 groups with 10 in each group. Preventive experiment: Adaptive f...
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Both NLRP3 inflammasome and chemokines are involved in the initiation and development of acute lung inflammation, but the underlying mechanism is still elusive. The present study investigated the role of chemokines and NLRP3 in recruiting neutrophils in the early phase of acute lung injury.
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In an endotoxin (lipopolys...
There is a well-known and established link between high lipopolysaccharide (LPS) levels in blood and the metabolic syndrome (MS). MS is a risk factor for developing severe COVID-19 and acute respiratory distress syndrome (ARDS). Here we define an interaction between SARS-CoV-2 Spike (S) protein and LPS and its link to aggravated inflammation in vit...
Citations
... The animal experiments were approved by the Experimental Animal Welfare and Ethics Committee of Putuo Hospital of Shanghai University of Chinese traditional Medicine (number: 17-08). The ARDS model was established as described in previous reports (Cleary et al., 2019;Huang et al., 2019) (Hou et al., 2014;Wei and Wang, 2017). Briefly, rats were randomized to two experimental groups (10 animals/group). ...
Background: The pathogenesis of COVID-19, including thrombocytopenia, has not been fully clarified. The lungs are a major organ of platelet production and thrombocytopenia induced by severe COVID-19 was proposed. Methods: the change of platelet level was analysed with clinical parameters in 95 hospitalized COVID-19 patients in Wuhan Third Hospital. The production of platelets in the lungs was explored in an ARDS rat model. Results: The level of platelets was negatively correlated with disease severity and was recovered with disease improvement. The non-survivors were accompanied by lower levels of platelet. The odds ratio (OR) of the valley level of the platelet count (PLTlow) was greater than 1, suggesting that PLTlow could be a death exposure factor. The platelet/lymphocyte ratio (PLR) was positively associated with severity of COVID-19, and the platelet/lymphocyte ratio threshold of 248.5 was best correlated with death risk (sensitivity 0.641 and specificity 0.815). To demonstrate the possible biogenesis aberration of platelet in lungs, an LPS-induced ARDS rat model was applied. Lower level of platelet in peripheral and less production of platelet from lungs in ARDS were demonstrated. Though megakaryocyte (MK) number in ARDS lungs is higher than controls, the immature platelet fraction (IPF) in postpulmonary blood is still at the same level as prepulmonary in ARDS rat, indicating that ARDS rats generated fewer platelets in lungs. Conclusion: Our data suggested that COVID-19-induced severe lung inflammation may impair platelet production in the lung. Thrombocytopenia may be mainly caused by platelet consumption for multiorgan thrombosis; however, biogenesis aberration of platelet in the lung induced by diffuse interstitial pulmonary damage cannot be ruled out.
... Previously, we demonstrated that SEW and FIR can significantly alleviate lung and tissue damage by decreasing inflammatory cell infiltration [11]. Experiments revealed that the protective effect of SEW and FIR on endotoxininduced ARDS may result from their role in reducing the levels of interleukin (IL)-1β and IL-6 in serum and the expression level of nuclear factor kappa-B (NF-κB) signaling pathways in lung tissue [12]. Other studies have reported that SEW and FIR have protective effects on lipopolysaccharide (LPS)induced ARDS in rats, which may be related to the increased expression of IL-4 in serum [13]. ...
Special electromagnetic field-treated water (SEW) and far-infrared radiation (FIR) can reduce acute respiratory distress syndrome (ARDS) in rats inflicted by lipopolysaccharides (LPSs). However, little is known about its underlying molecular mechanism. Differentially expressed proteins (DEPs) of SEW and FIR interventions were obtained from a proteomics database. A total of 89 DEPs were identified. Enrichment analysis of DEPs was performed using the Database for Annotation, Visualization, and Integrated Discovery. These DEPs were associated with the responses to LPSs, acute inflammation, extracellular exosomes, glucocorticoids, and electrical stimuli. The protein-protein interaction network was set up using the STRING database. Modular analysis was performed using MCODE in the Cytoscape software. Proteins Haptoglobin, Apolipoprotein B, Transthyretin, and Fatty acid binding protein 1 were among the core networks. A tail vein injection of LPS was used to establish the rat model with ARDS. Parallel reaction monitoring confirmed Hp protein expression. Inflammatory pathway factors were detected using an enzyme-linked immunosorbent assay. This indicates that SEW and FIR can be considered as potential clinical treatment methods for ARDS treatment and that their functional mechanisms are related to the ability of alleviating lung inflammation through Hp protein adjustment.
Introduction
Far-infrared radiation (FIR) is widely used in the treatment of various diseases such as insomnia and cardiovascular risk. Rheumatoid arthritis (RA) is a chronic systemic autoimmune disease in which the therapeutic potential of FIR in RA is unclear.
Objectives
To determine the therapeutic potential and mechanistic actions of FIR in treatment of RA.
Methods
Adjuvant-induced arthritis (AIA) rat models were established to assess the therapeutic potency of FIR in RA treatment. The scoring parameters such as arthritis score, swelling of the hind paw, spleen and thymus indices, micro-CT analysis indices were adopted to estimate the beneficial effects of FIR during RA treatment in AIA model. PCR gene expression arrays were used to analyze inflammatory and autoimmune genes expression profiles in rat synovium. The inflammatory and immunity genes profiling was further analyzed through transcription factor prediction using PROMO. A signaling network map of possible molecular circuits connecting the identified differential genes to the RA's pathogenesis was constructed based on extensive literature reviews, and the major signaling pathways were validated by Western blotting.
Results
Thirty minutes of FIR treatment significantly improved the symptoms of AIA in rats. Gene expression profiling indicated that 27 out of 370 genes were down-regulated by FIR. AP-1, CEBPα, CEBPβ, c-Fos, GR, HNF-3β, USF-1, and USF-2 were predicted as key transcription factors that regulated the identified differential genes. In addition, MAPK, PI3K-Akt, and NF-κB signaling are the major molecular pathways down-regulated by FIR treatment.
Conclusion
FIR may provide beneficial effects on the AIA rat model of arthritis by suppression of the MAPK, PI3K-Akt and NF-κB signaling pathways. Therefore, we believe that FIR may provide an alternative non-pharmacological and non-surgical therapeutic approach for the treatment of RA.
