One-step scaffold fabrication with live cell incorporation is a highly desirable technology for tissue engineering and regeneration. Projection stereolithography (PSL) represents a promising method owing to its fine resolution, high fabrication speed and computer-aided design (CAD) capabilities. However, the majority of current protocols utilize water-insoluble photoinitiators that are incompatible with live cell-fabrication, and ultraviolet (UV) light that is damaging to the cellular DNA. We report here the development of a visible light-based PSL system (VL-PSL), using lithium phenyl-2,4,6-trimethylbenzoylphosphinate (LAP) as the initiator and polyethylene glycol diacrylate (PEGDA) as the monomer, to produce hydrogel scaffolds with specific shapes and internal architectures. Furthermore, live human adipose-derived stem cells (hADSCs) were suspended in PEGDA/LAP solution during the PSL process, and were successfully incorporated within the fabricated hydrogel scaffolds. hADSCs in PEG scaffolds showed high viability (>90%) for up to 7 days after fabrication as revealed by Live/Dead staining. Scaffolds with porous internal architecture retained higher cell viability and activity than solid scaffolds, likely due to increased oxygen and nutrients exchange into the interior of the scaffolds. The VL-PSL should be applicable as an efficient and effective tissue engineering technology for point-of-care tissue repair in clinic.

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The Fuling (Poria cocos)-Guizhi (Cinnamomi ramulus) herb pair (FGHP) is a commonly used traditional Chinese herbal formula with coronary heart disease (CHD) treatment potential. However, the mechanism of FGHP in the treatment of CHD was still unclear. In this study, the action targets and underlying mechanism of FGHP against CHD were successfully achieved by combined network pharmacology prediction with experimental verification. 76 common targets were screened out by overlapping the chemical-protein data of FGHP and CHD-related targets. Then, two key targets were further selected for verification by using western blot analysis after analyzing PPI, GO function, and KEGG pathway. Results indicated FGHP could alleviate CHD syndromes and regulate inflammatory responses in acute myocardial ischemia rats, and the reduction of expression of TNF-α and IL-6 in myocardial tissue would be one of its possible underlying mechanisms. Our work demonstrated that network pharmacology combined with experimental verification provides a credible method to elucidate the pharmacological mechanism of FGHP against CHD.

Nephrotic syndrome (NS) is a clinical syndrome resulting from abnormal glomerular permeability, mainly manifesting as edema and proteinuria. Qingrekasen granule (QRKSG), a Chinese Uyghur folk medicine, is a single-flavor preparation made from chicory (Cichorium intybus L.), widely used in treating dysuria and edema. Chicory, the main component in QRKSG, effectively treats edema and protects kidneys. However, the active components in QRKSG and its underlying mechanism for treating NS remain unclear. This study explored the specific mechanism and composition of QRKSG on an NS rat model using integrated metabolomics and network pharmacology. First, metabolomics explored the relevant metabolic pathways impacted by QRKSG in the treatment of NS. Secondly, network pharmacology further explored the possible metabolite targets. Afterward, a comprehensive network was constructed using the results from the network pharmacology and metabolomics analysis. Finally, the interactions between the active components and targets were predicted by molecular docking, and the differential expression levels of the target protein were verified by Western blotting. The metabolomics results showed “D-Glutamine and D-glutamate metabolism” and “Alanine, aspartate, and glutamate metabolism” as the main targeted metabolic pathways for treating NS in rats. AKT1, BCL2L1, CASP3, and MTOR were the core QRKSG targets in the treatment of NS. Molecular docking revealed that these core targets have a strong affinity for flavonoids, terpenoids, and phenolic acids. Moreover, the expression levels of p-PI3K, p-AKT1, p-mTOR, and CASP3 in the QRKSG group significantly decreased, while BCL2L1 increased compared to the model group. These findings established the underlying mechanism of QRKSG, such as promoting autophagy and anti-apoptosis through the expression of AKT1, CASP3, BCL2L1, and mTOR to protect podocytes and maintain renal tubular function.

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