timosaponin-b-ii and Acute-Lung-Injury

timosaponin-b-ii has been researched along with Acute-Lung-Injury* in 1 studies

Other Studies

1 other study(ies) available for timosaponin-b-ii and Acute-Lung-Injury

Article	Year
Timosaponin B-II inhibits lipopolysaccharide-induced acute lung toxicity via TLR/NF-κB pathway. Toxicology mechanisms and methods, 2015, Volume: 25, Issue:9 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. Topics: Acute Lung Injury; Animals; Blotting, Western; Bronchoalveolar Lavage Fluid; Cytokines; Lipopolysaccharides; Lung; Male; Mice, Inbred BALB C; Saponins; Signal Transduction; Steroids; Toll-Like Receptor 2; Toll-Like Receptor 4; Transcription Factor RelA	2015

Article

Year

Timosaponin B-II inhibits lipopolysaccharide-induced acute lung toxicity via TLR/NF-κB pathway.

Toxicology mechanisms and methods, 2015, Volume: 25, Issue:9

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.

Topics: Acute Lung Injury; Animals; Blotting, Western; Bronchoalveolar Lavage Fluid; Cytokines; Lipopolysaccharides; Lung; Male; Mice, Inbred BALB C; Saponins; Signal Transduction; Steroids; Toll-Like Receptor 2; Toll-Like Receptor 4; Transcription Factor RelA

2015