98%
921
2 minutes
20
Cerebral ischemia reperfusion injury (CIRI) is a crucial process in the inflammatory response. Sodium danshensu (SDSS) is of protective effects in cardiovascular and cerebrovascular diseases due to its anti-inflammatory properties. Studies have demonstrated that SDSS administration reduces infarct volume, attenuates neurological impairment, and inhibits microglia activation in rat models of CIRI. While it is well established that miRNAs play roles in a wide range of diseases through multiple pathways. However, the mechanism by which SDSS alleviates inflammatory injury after CIRI and its potential interaction with miRNAs remain unclear. Thus, we aimed to investigate the effectiveness and mechanism of SDSS in CIRI, and to verify whether it exerts anti-inflammatory effects by affecting miRNA. Through bioinformatics analysis and experimental validation, we identified miR-130b-5p is a key gene in the CIRI process, with SDSS administration leading to an upregulation of miR-130b-5p that is indispensable for its anti-inflammatory effects. Moreover, both SDSS and miR-130b-5p reduced the expression of TLR4. Overall, the beneficial effects of SDSS on CIRI can be attributed to the up-regulation of miR-130b-5p and the inhibition of TLR4, resulting in the attenuation of the inflammatory response.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1016/j.intimp.2025.114497 | DOI Listing |
Chem Biodivers
September 2025
Zhejiang Provincial Engineering Research Center of New Technologies and Applications for Targeted Therapy of Major Diseases, Laboratory of Anti-Allergy Functional Compounds, College of Life Sciences and Medicine, Zhejiang Sci-Tech University, Hangzhou, China.
Autoimmune diseases (AIDs), defined by irregularities in immune system function, pose a substantial health challenge worldwide, impacting millions with persistent and frequently debilitating conditions. Conventional treatments, such as glucocorticoid-based immunosuppressive therapies, are associated with notable drawbacks and limitations. In response to these difficulties, recent scientific efforts have increasingly focused on natural compounds as potential therapeutic agents.
View Article and Find Full Text PDFACS Nano
September 2025
Department of Emergency and Critical Care Medicine, The Fourth Affiliated Hospital of Soochow University, Suzhou 215124, China.
Acute lung injury (ALI) is characterized by the excessive accumulation of reactive oxygen species (ROS), which triggers a severe inflammatory cascade and the destruction of the alveolar-capillary barrier, leading to respiratory failure and life-threatening outcomes. Considering the limitations and adverse effects associated with current therapeutic interventions, developing effective and safe strategies that target the complex pathophysiological mechanisms of ALI is crucial for improving patient outcomes. Herein, we developed an inhalable, multifunctional nanotherapeutic (MSCNVs@CAT) by encapsulating catalase (CAT) in mesenchymal-stem-cell-derived nanovesicles (MSCNVs).
View Article and Find Full Text PDFElife
September 2025
Department of Biology, University of Copenhagen, Copenhagen, Denmark.
Sickness-induced sleep is a behavior conserved across species that promotes recovery from illness, yet the underlying mechanisms are poorly understood. Here, we show that interleukin-6-like cytokine signaling from the gut to brain glial cells regulates sleep. Under healthy conditions, this pathway promotes wakefulness.
View Article and Find Full Text PDFJ Alzheimers Dis
September 2025
Amsterdam Public Health, Aging & Later life and Personalized Medicine, Amsterdam, the Netherlands.
BackgroundAllostatic load (AL), an umbrella term for the physiological response to chronic stress, is different in women and men. AL has also been associated with all-cause dementia.ObjectiveThe current study investigates if AL clusters differently in men and women, and if these sex-based clusters are associated with all-cause dementia.
View Article and Find Full Text PDFACS Chem Neurosci
September 2025
Department of Medical Biology, Faculty of Medicine, Bahçeşehir University, Istanbul 34353, Turkey.
IL-17A is a pro-inflammatory cytokine that significantly contributes to the pathogenesis of autoimmune diseases, including multiple sclerosis (MS). Previous studies have suggested that PARP-1 inhibitors can modulate IL-17A-mediated inflammation, prompting the investigation of Niraparib, an FDA-approved PARP-1 inhibitor, as a potential therapeutic agent for MS. In this study, we hypothesized that Niraparib could disrupt the interaction between IL-17A and its receptor, IL-17RA.
View Article and Find Full Text PDF