Publications by authors named "Sin-Hyang Park"
Background: Although copper oxide nanoparticles (CuONPs) offer certain benefits to humans, they can be toxic to organs and exacerbate underlying diseases upon exposure. Chronic obstructive pulmonary disease (COPD), induced by smoking, can worsen with exposure to various harmful particles. However, the specific impact of CuONPs on COPD and the underlying mechanisms remain unknown.
View Article and Find Full Text PDFAsian sand dust (ASD), a seasonal dust storm originating from the deserts of China and Mongolia, affects Korea and Japan during the spring, carrying soil particles and a variety of biochemical components. Exposure to ASD has been associated with the onset and exacerbation of respiratory disorders, although the underlying mechanisms remain unclear. This study investigates ASD-induced pulmonary toxicity and its mechanistic pathways, focusing on the role of thioredoxin-interacting protein (TXNIP).
View Article and Find Full Text PDFArticle Synopsis
- Copper oxide nanoparticles (CuO NPs) are increasingly used in various industries, raising concerns about their toxicity and potential to worsen asthma symptoms.
- A study using an asthma model showed that exposure to CuO NPs caused heightened inflammation, increased mucus production, and elevated levels of specific immune responses, all tied to the activation of the thioredoxin-interacting protein (TXNIP) pathway.
- Reducing TXNIP levels in experiments significantly lowered these adverse effects, indicating that targeting this pathway might help manage the pulmonary toxicity and asthma exacerbation caused by CuO NPs.
Silibinin Suppresses Inflammatory Responses Induced by Exposure to Asian Sand Dust.
Antioxidants (Basel)
September 2024
Article Synopsis
- * Silibinin treatment reduced inflammatory markers and improved oxidative stress responses in both cell lines and animal models exposed to ASD, showing significant decreases in various pro-inflammatory proteins.
- * The findings suggest that silibinin can alleviate pulmonary inflammation linked to ASD by targeting inflammatory signaling pathways and oxidative stress, highlighting its potential as a treatment option.