2020
DOI: 10.21037/atm-20-4233
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Abstract: Background: Pulmonary fibrosis (PF) is a fatal disease with increasing incidence. Ligustilide (LIG) has been shown to inhibit oxidative stress, apoptosis, and inflammation. Here we investigated the possible effect of LIG on bleomycin-induced PF in Sprague-Dawley rats.Methods: PF rats were set up through a single endotracheal injection of bleomycin (5 mg/kg). Then rats were treated with 20, 40, and 80 mg/kg LIG for four weeks, and the effects were estimated.Results: Overall, LIG significantly improved ventilati… Show more

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Cited by 20 publications
(9 citation statements)
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“…The early stage of IPF is manifested inflammation, especially in the mouse model after BLM for 7 days. According to recent studies and our results, the TLR4/MyD88/NF- κ B p65 signaling pathway appears to have potential functions in IPF [ 18 , 31 ]. In our study, some compounds in the WBT formula have been shown to inhibit the TLR4/MyD88/NF- κ B pathway.…”
Section: Discussionsupporting
confidence: 71%
See 1 more Smart Citation
“…The early stage of IPF is manifested inflammation, especially in the mouse model after BLM for 7 days. According to recent studies and our results, the TLR4/MyD88/NF- κ B p65 signaling pathway appears to have potential functions in IPF [ 18 , 31 ]. In our study, some compounds in the WBT formula have been shown to inhibit the TLR4/MyD88/NF- κ B pathway.…”
Section: Discussionsupporting
confidence: 71%
“…Makino, which reduces inflammatory cytokines and oxidative stress to protect acute lung injury in mice model by regulating the NF- κ B pathway [ 15 17 ]. A bioactive compound from Ligusticum striatum DC., ligustilide, can suppress oxidative stress and inflammation to avoid BLM-induced PF in rat model through the inhibition of the TLR4/MyD88/NF- κ B pathway [ 18 ]. However, the protective effects and possible mechanisms of the WBT formula in the early phase of IPF, especially the inflammatory process, have not been thoroughly explored.…”
Section: Introductionmentioning
confidence: 99%
“…Inflammatory fibroblasts persistently activate the fibroblasts in an autocrine/paracrine manner in the lungs, resulting in pulmonary fibrosis (63)(64)(65). The proinflammatory role of TLR4-MD2 complex and Myd88 signaling pathway in the lungs has also been evaluated (66)(67)(68)(69) and associated with the fibrotic process leading to pulmonary fibrosis (60,(70)(71)(72)(73)(74). In our study, we found that eCIRP induces proinflammatory cytokines and their pathways in pulmonary fibroblasts in a TLR4 dependent manner.…”
Section: Discussionsupporting
confidence: 54%
“…No reuse allowed without permission. TLR4/MyD88/NF-κB(p65) signal pathway activation has great significance in inflammation and fibrosis processes [16][17][18]. Some studies reveal ILK could effectively regulate this pathway [19].…”
Section: Discussionmentioning
confidence: 99%