Biomol Ther.  2024 Jan;32(1):162-169. 10.4062/biomolther.2023.187.

Therapeutic Effects of (+)-Afzelechin on Particulate Matter-Induced Pulmonary Injury

• Cho S
• Park YJ
• Bae JS

• KMID: 2550268
• DOI: http://doi.org/10.4062/biomolther.2023.187

Abstract

Particulate matter (PM) constitutes a hazardous blend of organic and inorganic particles that poses health risks. Inhalation of fine airborne PM with a diameter of ≤ 2.5 μm (PM_2.5 ) can lead to significant lung impairments. (+)-afzelechin (AZC), a natural com-pound sourced from Bergenia ligulata, boasts a range of attributes, including antioxidant, antimicrobial, anticancer, and cardio-vascular effects. However, knowledge about the therapeutic potential of AZC for patients with PM_2.5 -induced lung injuries remains limited. Thus, in this study, we investigated the protective attributes of AZC against lung damage caused by PM_2.5 exposure. AZC was administered to the mice 30 min after intratracheal instillation of PM_2.5 . Various parameters, such as changes in lung tissue wet/dry (W/D) weight ratio, total protein/total cell ratio, lymphocyte counts, levels of inflammatory cytokines in bronchoalveolar lavage fluid (BALF), vascular permeability, and histology, were evaluated in mice exposed to PM_2.5 . Data demonstrated that AZC mitigated lung damage, reduced W/D weight ratio, and curbed hyperpermeability induced by PM_2.5 exposure. Furthermore, AZC effectively lowered plasma levels of inflammatory cytokines produced by PM_2.5 exposure. It reduced the total protein concentration in BALF and successfully alleviated PM_2.5 -induced lymphocytosis. Additionally, AZC substantially diminished the expression levels of Toll-like receptors 4 (TLR4), MyD88, and autophagy-related proteins LC3 II and Beclin 1. In contrast, it elevated the protein phosphorylation of the mammalian target of rapamycin (mTOR). Consequently, the anti-inflammatory attribute of AZC positions it as a promising therapeutic agent for mitigating PM_2.5 -induced lung injuries by modulating the TLR4–MyD88 and mTOR–au- tophagy pathways.

Keyword

(+)-afzelechin; Particulate matter; Lung injury; TLR4–mTOR–autophagy pathway