Therapeutic effects of Saikosapoin D on bleomycininduced pulmonary fibrosis in mice via regulation of IL- 33/ST2 pathway

Xu, Jiao; Miao, Xiaoqing; Zheng, Jie; Ding, Mingchao; Zhuang, Zhi-fang

doi:10.4314/tjpr.v16i3.12

Cited by 1 publication

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“…Pulmonary fibrosis is characterized by chronic and invasive scar formation and deposition of extracellular matrix (ECM), followed by death due to impaired lung function and respiratory failure [10]. Studies have shown that increased epithelial-mesenchymal transition (EMT) and perturbation of the matrix synthesis/degradation balance are the driving factors in PF [11,12].…”

Section: Discussionmentioning

confidence: 99%

Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway

Ma¹,

Shi²,

Wei³

et al. 2020

Trop. J. Pharm Res

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Purpose: To investigate the therapeutic effect of loureirin B (LB) on amiodarone (AD)-induced pulmonary fibrosis (PF).Methods: Forty-eight male C57BL/6 mice, 8–10 weeks of age, were divided into four groups (n=12). Oral administration of amiodarone hydrochloride (AD) was performed for 4 weeks to induce pulmonary fibrosis. The degree of fibrosis was assessed by Masson staining, while collagen I and α-smooth muscle actin (α-SMA) levels were evaluated by Western blot analysis. ELISA was used to measure the levels of cytokines TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid (BALF) and lung tissue. Levels of p- Smad2, Smad2, p-Smad3 and Smad3 were determined by western blotting.Results: AD treatment increased the collagen levels and expression levels of collagen I and α-smooth muscle actin (α-SMA) in lung tissue and of inflammatory cytokines TNF-α, IL-1β, and IL-6, in both bronchoalveolar lavage fluid (BALF) and lung tissue in a dose-dependent manner (p < 0.01).Furthermore, AD increased the levels of p-Smad2/3. AD-induced increases in collagen I and α-SMA levels were reversed by loureirin B (LB). In addition, LB reduced AD-induced increased levels of the inflammatory cytokines TNF-α, IL-1β, and IL-6 in both bronchoalveolar lavage fluid (BALF) and lung tissue (p < 0.01).Conclusion: These results demonstrate that LB downregulates expression of fibrosis-related proteins and suppresses AD-induced PF. The mechanism responsible for the protective effect of LB on ADinduced PF might involve inhibition of the Smad2/3 pathway. Thus, LB is a potential therapeutic agent for the management of PF. Keywords: Amiodarone, Loureirin B, Pulmonary fibrosis, Smad, Inflammation

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Section: Discussionmentioning

confidence: 99%

Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway

Ma¹,

Shi²,

Wei³

et al. 2020

Trop. J. Pharm Res

View full text Add to dashboard Cite

show abstract

Therapeutic effects of Saikosapoin D on bleomycininduced pulmonary fibrosis in mice via regulation of IL- 33/ST2 pathway

Abstract: Purpose: To investigate the therapeutic effects of saikosapoin D (SSD) on bleomycin (BLM)-induced pulmonary fibrosis (PF) in mice and its probable mechanisms. Methods: PF mice were prepared by intraperitoneal (i.p.) injection of BLM (5 mg/kg

Cited by 1 publication

References 20 publications

Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway

Loureirin B attenuates amiodarone-induced pulmonary fibrosis by suppression of TGFβ1/Smad2/3 pathway

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