Pycnogenol-Assisted Alleviation of Titanium Dioxide Nanoparticle-Induced Lung Inflammation via Thioredoxin-Interacting Protein Downregulation

• Published in: Antioxidants Vol. 13; no. 8; p. 972
• Main Authors: Lim, Je-Oh, Kim, Woong-Il, Pak, So-Won, Lee, Se-Jin, Moon, Changjong, Shin, In-Sik, Kim, Sung-Hwan, Kim, Jong-Choon
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 09.08.2024; MDPI
• Subjects: Antioxidants; antioxidative effect; Apoptosis; Asthma; Biocompatibility; Caspase-3; Cell cycle; Chronic obstructive pulmonary disease; Complications and side effects; Cytotoxicity; Diagnosis; Dosage and administration; Down-regulation; Epithelial cells; Gene expression; Glutathione; Health aspects; Identification and classification; Inflammation; Kinases; Laboratory animals; Lung diseases; lung inflammation; Lungs; mRNA; Nanomaterials; Nanoparticles; Ostomy; Oxidative stress; Physiological aspects; Prevention; Protein expression; Proteins; Pycnogenol; Respiratory tract; Risk factors; Structure; Testing; Thioredoxin; thioredoxin-interacting protein; Titanium; Titanium dioxide; titanium dioxide nanoparticle; Toxicity; Tumor necrosis factor-TNF; South Korea; St Louis Missouri; France; Ann Arbor Michigan; United States > US; pycnogenol; thioredoxin-interacting protein; antioxidative effect; titanium dioxide nanoparticle; lung inflammation
• ISSN: 2076-3921; 2076-3921
• DOI: 10.3390/antiox13080972

Titanium dioxide nanoparticles (TiO NPs) are used in products that are applied to the human body, such as cosmetics and food, but their biocompatibility remains controversial. Pycnogenol (PYC), a natural extract of pine bark, exerts anti-inflammatory and antioxidant effects. In this study, we investigated whether PYC effectively alleviates pulmonary toxicity induced by airway exposure to TiO NPs, and the beneficial effects of PYC were explained through the analysis of changes to the mechanism of cytotoxicity. TiO NPs induced pulmonary inflammation and mucus production, increased the levels of malondialdehyde, and upregulated thioredoxin-interacting protein (TXNIP) and cleaved-caspase 3 (Cas3) in the lungs of mice. However, PYC treatment reduced the levels of all toxicity markers of TiO NPs and restored glutathione levels. These antioxidant and anti-inflammatory effects of PYC were also demonstrated in TiO NP-exposed human airway epithelial cells by increasing the mRNA levels of antioxidant enzymes and decreasing the expression of TXNIP, cleaved-Cas3, and inflammatory mediators. Taken together, our results showed that PYC attenuated TiO NP-induced lung injury via TXNIP downregulation. Therefore, our results suggest the potential of PYC as an effective anti-inflammatory and antioxidant agent against TiO NP-induced pulmonary toxicity.