IRANIAN POLYMER JOURNAL
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2024
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IF 2.4
Yang Guoqian,Liu Mengmeng,Su Yingfeng,Yu Chi
Amidst the relentless innovation in materials science and bone tissue engineering, the quest for next-generation bone graft materials with bespoke functionalities has emerged as a pivotal research domain. This study produced and characterized a novel bone healing material. First, we explained how three-armed polylactic acid (3s-PLA) was created in supercritical carbon dioxide (ScCO 2 ) and utilized as a matrix material. Following that, we described how the solution blending approach was employed to create three-armed polylactic acid/chitosan/nanohydroxyapatite (3s-PLA/CS/nHA) composites. The composites were then drug-loaded with prednisone acetate as a model drug utilizing the supercritical impregnation technique. Ultimately, the Ritger-Peppas model was substantially followed by the drug release of the drug-loaded composites when the in vitro drug-release kinetics of the drug-loaded materials were investigated. The porous structure of 3s-PLA was demonstrated by differential scanning calorimetry (DSC), Fourier transform infrared spectroscopy (FTIR), and nuclear magnetic resonance (NMR) hydrogen spectroscopy. Morphologic studies using scanning electron microscopy (SEM) revealed the homogeneous distribution of drug in the matrix of the mixtures as well as the porous structure of 3s-PLA and 3s-PLA/CS/nHA. The hydrophilicity of 3s-PLA/CS/nHA was examined by the use of water contact angle (WCA), revealing that the material in question has a hydrophilic water contact angle of 45.69°. Furthermore, research was conducted using one-way tests and investigations to characterize in vitro drug-release carrier materials under various drug conditions and temperatures. The carrier material consistently released up to 84.8% of prednisone acetate over the course of 72 h, demonstrating good control over prolonged release, according to the results. Graphical abstract
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产品关联
DOI
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Yufeng Yao,Lijun Shao,Ziqi Li,Jiahao Liang,Chenchen Zhu,Shumei Wang,Chaozhan Lin,Fangle Liu
Background Interstitial pneumonia, particularly usual interstitial pneumonia (UIP) and idiopathic pulmonary fibrosis (IPF), is a disease with progressive and fatal disorder, and limited treatment options. Xiebai San (XBS), a classical Chinese herbal formula, has shown clinical promise but its mechanism of action remains unclear. Purpose To clarify the effects and mechanism of XBS on interstitial pneumonia. Methods The in vivo pharmacochemical analysis (UPLC-Q-Exactive-Orbitrap MS/MS), network pharmacology, and GEO database analysis (GSE10667) were applied to predict potential targets of XBS on interstitial pneumonia. BLM-induced mice received XBS (1.4, 2.8, 5.6 g/kg) or dexamethasone (0.5 mg/kg) for 21 days. Lung index, histopathology observation (H&E, Collagen-1 IHC), pulmonary function, and biomarkers of inflammation, oxidative stress and fibrosis were used to evaluated the efficacy of XBS. Reverse-phase protein microarray (RPPM), RT-qPCR, and Western blotting were integrated to clarify its mechanism. Results Thirty-seven components of XBS were identified in vivo , and they were associated with 237 potential targets for interstitial pneumonia. And GEO analysis confirmed the upregulation of key nodes (NCOA2, ESR1, and ESR2) in patients. XBS significantly attenuated BLM-induced lung damage, evidenced by reduced lung index, improved pulmonary function (Penh, EEP, PIF, PEF), decreased inflammatory infiltrates, collagen deposition, and alveolar destruction. XBS suppressed proinflammatory cytokines (TNF-α, IL-1β), oxidative stress (MDA, MPO), restored antioxidants (GSH, SOD), and inhibited fibrotic factors (TGF-β1, α-SMA, Collagen-1/3). Mechanistically, XBS downregulated the mRNA and protein expression of NCOA2 and ESR1/2, subsequently inhibiting glycolytic metabolic reprogramming (G6PC, PFKFB3, HIF-1α) and the TGF-β1/ERK1/2-Smad7 pro-fibrotic signaling pathway. Conclusion XBS alleviates BLM-induced interstitial pneumonia via NCOA2-ESR1/2-driven glycolytic metabolic reprogramming and TGF-β1/ERK1/2-Smad7 fibrotic signaling, offering a mechanistic rationale for interstitial pneumonia.
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产品关联
DOI
PubMed
高影响因子
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