PMID- 38148560
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240105
IS  - 1976-9148 (Print)
IS  - 2005-4483 (Electronic)
IS  - 1976-9148 (Linking)
VI  - 32
IP  - 1
DP  - 2024 Jan 1
TI  - Therapeutic Effects of (+)-Afzelechin on Particulate Matter-Induced Pulmonary 
      Injury.
PG  - 162-169
LID - 10.4062/biomolther.2023.187 [doi]
AB  - 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 mum (PM(2.5)) can lead to significant lung impairments. (+)-afzelechin 
      (AZC), a natural compound sourced from Bergenia ligulata, boasts a range of 
      attributes, including antioxidant, antimicrobial, anticancer, and cardiovascular 
      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-autophagy pathways.
FAU - Cho, Sanghee
AU  - Cho S
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Republic of Korea.
FAU - Park, Yun Jin
AU  - Park YJ
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Republic of Korea.
FAU - Bae, Jong-Sup
AU  - Bae JS
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Republic of Korea.
LA  - eng
PT  - Journal Article
PL  - Korea (South)
TA  - Biomol Ther (Seoul)
JT  - Biomolecules & therapeutics
JID - 101472832
PMC - PMC10762276
OTO - NOTNLM
OT  - (+)-afzelechin
OT  - Lung injury
OT  - Particulate matter
OT  - TLR4-mTOR-autophagy pathway
COIS- CONFLICT OF INTEREST The authors have no conflicts of interest to declare.
EDAT- 2023/12/27 06:41
MHDA- 2023/12/27 06:42
PMCR- 2024/01/01
CRDT- 2023/12/27 00:43
PHST- 2023/10/30 00:00 [received]
PHST- 2023/11/14 00:00 [revised]
PHST- 2023/11/15 00:00 [accepted]
PHST- 2023/12/27 06:42 [medline]
PHST- 2023/12/27 06:41 [pubmed]
PHST- 2023/12/27 00:43 [entrez]
PHST- 2024/01/01 00:00 [pmc-release]
AID - biomolther.2023.187 [pii]
AID - bt-32-1-162 [pii]
AID - 10.4062/biomolther.2023.187 [doi]
PST - ppublish
SO  - Biomol Ther (Seoul). 2024 Jan 1;32(1):162-169. doi: 10.4062/biomolther.2023.187.