Sparganii Rhizoma alleviates pulmonary fibrosis by inhibiting fibroblasts differentiation and epithelial-mesenchymal transition mediated by TGF-β1/ Smad2/3 pathway

Liu, Jing; Gao, Dongyang; Ding, Qi; Zhang, Binbin; Zhu, Wenxiang; Shi, Yuanyuan

doi:10.1016/j.jep.2023.116305

Cited by 2 publications

(2 citation statements)

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“…IPF is a chronic progressive disease with the development of interstitial fibrosis and progressive respiratory failure [ 2 , 31 ]. In most cases, the prognosis of IPF is unfavorable, with an average life expectancy of about five years from diagnosis [ 5 ]. Current therapies, Nintedanib and pirfenidone, slow progression by preserving lung function.…”

Section: Discussionmentioning

confidence: 99%

“…Currently, the incidence and prevalence of IPF are increasing worldwide [ 3 , 4 ]. The median survival of patients with IPF is 3–5 years [ 5 ]. Fibrogenesis in IPF is known to be mainly mediated by abnormal release of profibrogenic factors such as tumor necrosis factor-α (TNF-α) and interleukin 1β (IL-1β), which promote myofibroblast differentiation/activation, transforming growth factor-beta (TGF-β) [ 2 ] and extracellular matrix (ECM) deposition [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Anti-Inflammatory and Antifibrotic Potential of Longidaze in Bleomycin-Induced Pulmonary Fibrosis

Pakhomova,

Pershina,

Bochkov

et al. 2023

Life

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Idiopathic pulmonary fibrosis (IPF) is one of the most common forms of interstitial lung disease, characterized by progressive parenchymal fibrosis and respiratory failure. In a model of bleomycin-induced pulmonary fibrosis, the antifibrotic and anti-inflammatory activity of Longidaze (Bovhyaluronidase Azoxymer), which contains a conjugate of the hyaluronidase enzyme with a high molecular weight synthetic carrier azoxymer bromide, was investigated. Experiments were conducted in male C57BL/6 mice. Longidaze was administered at different doses by intranasal and intramuscular routes. Histology, hematology, and enzyme-linked immunosorbent assay were used in the study. The use of Longidaze reduced pulmonary fibrosis, as evidenced by an improvement in histopathologic damage to the lungs, a decrease in the area of connective tissue, and the levels of profibrotic factors (TGF-β1, hydroxyproline, collagen I) in lung tissue. In addition, Longidaze inhibited the inflammatory response in pulmonary fibrosis, and decreased the levels of IL-6, TNF-α, and hyaluronic acid in lung tissue and the recruitment of inflammatory cells into lung tissue. The highest therapeutic efficacy was observed with the use of Longidaze at doses of 120 and 1200 U/kg intramuscularly, which was superior to that of the reference drug pirfenidone axunio. The data presented in this study suggest that Longidaze is a new and promising drug for the treatment of IPF that warrants further investigation in patients with fibrotic interstitial lung disease.

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Section: Discussionmentioning

confidence: 99%