Atherosclerosis is a complex metabolic disease characterized by the dysfunction of lipid metabolism and chronic inflammation in the intimal space of the vessel. As the most abundant innate immune cells, monocyte-derived macrophages play a pivotal role in the inflammatory response, cholesterol metabolism, and foam cell formation. In recent decades, it has been demonstrated that monocytes and macrophages can establish innate immune memory (also termed trained immunity) via endogenous and exogenous atherogenic stimuli and exhibit a long-lasting proinflammatory phenotype. The important cellular metabolism processes, including glycolysis, oxidative phosphorylation (OXPHOS), the tricarboxylic acid (TCA) cycle, fatty acid synthesis, and cholesterol synthesis, are reprogrammed. Trained monocytes/macrophages with innate immune memory can be persistently hyperactivated and can undergo extensive epigenetic rewiring, which contributes to the pathophysiological development of atherosclerosis via increased proinflammatory cytokine production and lipid accumulation. Here, we provide an overview of the regulation of cellular metabolic processes and epigenetic modifications of innate immune memory in monocytes/macrophages as well as the potential endogenous and exogenous stimulations involved in the progression of atherosclerosis that have been reported recently. These elucidations might be beneficial for further understanding innate immune memory and the development of therapeutic strategies for inflammatory diseases and atherosclerosis.
A new indole-diterpenoid, penijanthine E (1), and a known analogue (2), were obtained from the PDB culture of the marine-derived fungus Penicillium citrinum ZSS-9. The absolute configuration of 1 was elucidated by calculated TDDFT ECD and DP4plus calculations. The absolute configuration of 2 was confirmed by single-crystal X-ray diffraction analysis and TDDFT ECD calculations. Compounds 1 and 2 showed antiviral activity against influenza A virus (IAV) of A/WSN/33(H1N1) and A/PR/8/34(H1N1) strains with IC 50 values ranging from 12.6 to 46.8 μM.
Background: Unilateral double-port endoscopic (UBE) discectomy is a newly invented surgical procedure for the treatment of lumbar disc herniation (LDH). As it has been on the market for a relatively short period of time, the lack of systematic analysis of the clinical efficacy and safety of the treatment of LDH is unclear.In this study, we compare randomised controlled trials to assess the clinical efficacy and safety of UBE and conventional endoscopic discectomy for LDH. Methods:The Chinese National Knowledge Infrastructure, Wanfang, PubMed, Embase, Cochrane library, and Chinese Biomedical databases were searched (from database inception to October 2022). The quality of included studies was assessed according to the Cochrane Risk Manual. The intervention of the UBE group was UBE discectomy, and the control measure was conventional endoscopic discectomy. The outcome indicators included hospital stay, the visual analogue score (VAS), intraoperative bleeding, the Oswestry dysfunction index (ODI), and complications. The data were analyzed using RevMan 5.4. Results:In total, 7 studies were included. Intraoperative bleeding was higher in the control group than in the UBE group (MD =−0.07; 95% confidence interval (CI): −0.21 to 0.08; P=0.14). The improvement of ODI score in the UBE group was significantly better (MD =0.13, 95% CI: −0.06 to 0.32; P=0.17). There was no statistical heterogeneity in terms of postoperative complications (I 2 =0%, P=1.00). The complication rate in the UBE group was lower (MD =0; 95% CI: −0.15 to 0.15; P=1.00). Postoperative VAS improvement in UBE group was significantly better (MD =−0.12; 95% CI: −0.27 to 0.03; P=0.11). The length of hospital stay in UBE group was shorter (MD =−2.04; 95% CI: −2.23 to −1.84; P<0.05). The t value of hospitalization length, VAS, Intraoperative bleeding, ODI and complicationswere 0.000-0.081, v was 20-26, all P>0.05, suggesting that this conclusion was stable.Conclusions: Patients in the UBE group spent less time in the hospital than the control group, and UBE group patients also woke up earlier than the control group. Therefore, UBE discectomy has certain reference value and can be popularized in clinic.
Aim: To explore the effect of miR-125b-5p/nuclear factor of activated T cells 1 ( NFAT2)/ F2RL2 on myocardial infarction (MI). Method: After establishment of MI mouse model and oxygen glucose deprivation (OGD)-induced cell model, the effects of NFAT2 on the process of MI were observed, the effects of miR-125b-5p/ NFAT2/ F2RL2 on the cell viability, apoptosis, and inflammatory factors levels were determined. Result: NFAT2 silencing relieved MI and inhibited the inflammation in MI model mice. In OGD-induced human coronary artery endothelial cells and human cardiac microvascular endothelial cells, miR-125b-5p enhanced cell viability, yet repressed cell apoptosis and inflammatory factors and NFAT2 levels. NFAT2 overexpression reversed the effects of miR-125b-5p, while F2RL2 silencing offset the effects of NFAT2 overexpression. Conclusion: MiR-125b-5p alleviates MI injury by inhibiting NFAT2 level to reduce F2RL2 expression.
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