In:
PLOS ONE, Public Library of Science (PLoS), Vol. 17, No. 10 ( 2022-10-26), p. e0275748-
Abstract:
Negative air ions (NAIs) being bioactive and negative charged molecules may confer antioxidant and anti-inflammatory activity. We assessed the effect of NAIs on two inflammatory diseases in animal models including lipopolysaccharide (LPS) induced acute lung injury (ALI) and wound healing in diabetic rats. We used intra-tracheal infusion of LPS to induce ALI and made a full-thickness cutaneous wound in streptozotocin-induced diabetic female Wistar rats. We evaluated NAIs effects on reactive oxygen species amount, leukocyte infiltration, wound healing rate, western blot, and immunohistochemistry in the lungs of ALI and skin sections of wounds. Our data found NAIs exposed saline displayed higher antioxidant activity vs. non-exposed saline. NAIs exposure did not significantly affect arterial blood pressure and respiratory frequency in control and LPS treated groups. LPS increased leukocyte infiltration, caspase 3/Poly-ADP-ribose-polymerase-mediated apoptosis formation and decreased Beclin-1/LC3-II-mediated autophagy in lungs. NAIs exposure conferred pulmonary protection by depressed leukocyte infiltration and caspase 3/Poly-ADP-ribose-polymerase mediated apoptosis and enhanced LC3-II-mediated autophagy in LPS induced ALI. NAIs treatment resulted in a significantly accelerated wound closure rate, decreased erythrocyte accumulation and leukocyte infiltration mediated oxidative stress and inflammation, and upregulated expression of skin collagen, vascular endothelial growth factor receptor-2 (VEGFR-2) and factor transforming growth factor-beta 1 (TGF-β1) vs non-treated group. Based on these results, it is suggested that NAIs conferred a protection through the upregulating LC3-II-dependent autophagy mechanism and downregulating leukocyte infiltration mediated inflammation and caspase 3/Poly-ADP-ribose-polymerase signaling in the LPS-treated ALI and promoted diabetic wound healing through the enhancing skin collagen synthesis, VEGFR-2 and TGF-β1 pathways.
Type of Medium:
Online Resource
ISSN:
1932-6203
DOI:
10.1371/journal.pone.0275748
DOI:
10.1371/journal.pone.0275748.g001
DOI:
10.1371/journal.pone.0275748.g002
DOI:
10.1371/journal.pone.0275748.g003
DOI:
10.1371/journal.pone.0275748.g004
DOI:
10.1371/journal.pone.0275748.g005
DOI:
10.1371/journal.pone.0275748.g006
DOI:
10.1371/journal.pone.0275748.g007
DOI:
10.1371/journal.pone.0275748.g008
DOI:
10.1371/journal.pone.0275748.g009
DOI:
10.1371/journal.pone.0275748.g010
DOI:
10.1371/journal.pone.0275748.g011
DOI:
10.1371/journal.pone.0275748.s001
DOI:
10.1371/journal.pone.0275748.r001
DOI:
10.1371/journal.pone.0275748.r002
DOI:
10.1371/journal.pone.0275748.r003
DOI:
10.1371/journal.pone.0275748.r004
Language:
English
Publisher:
Public Library of Science (PLoS)
Publication Date:
2022
detail.hit.zdb_id:
2267670-3
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