PMID- 36430427
OWN - NLM
STAT- MEDLINE
DCOM- 20221129
LR  - 20221214
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 23
IP  - 22
DP  - 2022 Nov 12
TI  - Cirsilineol Treatment Attenuates PM(2.5)-Induced Lung Injury in Mice.
LID - 10.3390/ijms232213948 [doi]
LID - 13948
AB  - Ultrafine particulate matter with less than 2.5 mum diameter (PM(2.5)) is an air 
      pollutant that causes severe lung damage. Currently, effective treatment and 
      preventive methods for PM(2.5)-induced lung damage are limited. Cirsilineol (CSL) 
      is a small natural compound isolated from Artemisia vestita. In this study, the 
      efficacy of CSL on PM(2.5)-induced lung toxicity was tested, and its mechanism 
      was identified. Lung injury was caused by intratracheal administration of PM(2.5) 
      suspension in animal models. Two days after PM(2.5) pretreatment, CSL was 
      injected via mouse tail vein for two days. The effects of CSL on PM(2.5)-induced 
      lung damage, autophagy, apoptosis, and pulmonary inflammation in a mouse model 
      and their mechanisms were investigated. CSL significantly suppressed histological 
      lung damage and lung wet/dry weight proportion. CSL also significantly reduced 
      PM(2.5)-induced autophagy dysfunction, apoptosis, lymphocyte suppression, and 
      inflammatory cytokine levels in bronchoalveolar fluid (BALF). Furthermore, CSL 
      increased mammalian target of rapamycin (mTOR) phosphorylation and significantly 
      inhibited the expression of Toll-like receptors (TLR) 2 and 4, MyD88, and the 
      autophagy proteins, Beclin1 and LC3II. Thus, CSL exerts protective effects on 
      pulmonary damage by regulating mTOR and TLR2,4-myD88 autophagy pathways. 
      Therefore, CSL can be used as an effective treatment for PM(2.5)-induced lung 
      damage.
FAU - Kim, Chaeyeong
AU  - Kim C
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Korea.
FAU - Kim, Go Oun
AU  - Kim GO
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Korea.
FAU - Bae, Jong-Sup
AU  - Bae JS
AUID- ORCID: 0000-0002-5756-9367
AD  - College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook 
      National University, Daegu 41566, Korea.
LA  - eng
GR  - HI15C0001/Korea Health Technology R&D Project through the Korea Health 
      Industry Development Institute (KHIDI), funded by the Ministry of Health & 
      Welfare, Republic of Korea/
GR  - 2020R1A2C1004131 and 2022R1A4A10189001/National Research Foundation of Korea 
      (NRF) grant funded by the Korean government (MSIT)/
PT  - Journal Article
DEP - 20221112
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 41365-32-6 (cirsilineol)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Particulate Matter)
SB  - IM
MH  - Mice
MH  - Animals
MH  - *Lung Injury/chemically induced/drug therapy
MH  - Myeloid Differentiation Factor 88
MH  - TOR Serine-Threonine Kinases
MH  - Particulate Matter/toxicity
MH  - Disease Models, Animal
MH  - Mammals
PMC - PMC9692977
OTO - NOTNLM
OT  - 4-mTOR autophagy
OT  - TLR2
OT  - apoptosis
OT  - cirsilineol
OT  - lung toxicity
OT  - particulate matter
COIS- The authors declare no conflict of interest.
EDAT- 2022/11/27 06:00
MHDA- 2022/11/30 06:00
PMCR- 2022/11/12
CRDT- 2022/11/26 01:16
PHST- 2022/10/08 00:00 [received]
PHST- 2022/10/30 00:00 [revised]
PHST- 2022/11/10 00:00 [accepted]
PHST- 2022/11/26 01:16 [entrez]
PHST- 2022/11/27 06:00 [pubmed]
PHST- 2022/11/30 06:00 [medline]
PHST- 2022/11/12 00:00 [pmc-release]
AID - ijms232213948 [pii]
AID - ijms-23-13948 [pii]
AID - 10.3390/ijms232213948 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Nov 12;23(22):13948. doi: 10.3390/ijms232213948.