Abstract |
Timosaponin B-II (TB), a main bioactive compound in Anemarrhena asphodeloides Bunge, has various kinds of pharmacological activities, the present study aimed to investigate the protective role of TB on lipopolysaccharide (LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS, and TB (20 and 60 mg/kg) was given orally 1 h prior to LPS administration. After 6 h, bronchoalveolar lavagefluid (BALF) and lung tissue were collected. TB decreased LPS-induced evident lung histopathological changes, lung wet-to-dry weight (W/D) ratio and lung myeloperoxidase (MPO) activity. In addition, TB inhibited inflammatory cells and cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in BALF. Furthermore, we demonstrated that TB inhibited the Toll-like receptor-2 (TLR2), Toll-like receptor-4 (TLR4), myeloid differentiation primary response gene-88 (MyD88), nuclear factor-κB (NF-κB) p65 in LPS-induced ALI. These results showed that administration of TB prior to LPS improves ALI, possibly mediating ALI through suppressing TLR/NF-κB pathway activation.
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Authors | Tianzhu Zhang, Jing Wang, Shumin Wang, Chunhua Ma |
Journal | Toxicology mechanisms and methods
(Toxicol Mech Methods)
Vol. 25
Issue 9
Pg. 665-71
( 2015)
ISSN: 1537-6524 [Electronic] England |
PMID | 26540118
(Publication Type: Journal Article)
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Chemical References |
- Cytokines
- Lipopolysaccharides
- Saponins
- Steroids
- Tlr2 protein, mouse
- Tlr4 protein, mouse
- Toll-Like Receptor 2
- Toll-Like Receptor 4
- Transcription Factor RelA
- lipopolysaccharide, E coli O55-B5
- timosaponin B-II
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Topics |
- Acute Lung Injury
(chemically induced, metabolism, pathology, prevention & control)
- Animals
- Blotting, Western
- Bronchoalveolar Lavage Fluid
(cytology, immunology)
- Cytokines
(metabolism)
- Lipopolysaccharides
(toxicity)
- Lung
(drug effects, immunology, metabolism, pathology)
- Male
- Mice, Inbred BALB C
- Saponins
(administration & dosage, therapeutic use)
- Signal Transduction
(drug effects)
- Steroids
(administration & dosage, therapeutic use)
- Toll-Like Receptor 2
(antagonists & inhibitors)
- Toll-Like Receptor 4
(antagonists & inhibitors)
- Transcription Factor RelA
(antagonists & inhibitors)
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