Seven extraction methods, including hot water extraction (HWE), pressurized water extraction (PWE), ultrasound-assisted extraction, microwave-assisted extraction, ultrasound-assisted enzymatic extraction, high-speed shearing homogenization extraction, and ultrasound-microwave-assisted extraction, were utilized to extract polyphenolic-protein-polysaccharide complexes (PPPs) from Hovenia dulcis. Next, their physicochemical properties and in vitro antioxidant activities, antiglycation effects, and inhibition activities on α-glucosidase and α-amylase were studied and compared. The findings from this study indicate that various extraction processes exhibit notable influences on the physicochemical properties and in vitro bioactivities of PPPs. Extraction yields, contents of polyphenolics and flavonoids, apparent viscosities, molecular weights, molar ratios of monosaccharide compositions, and ratios of amino acid compositions in PPPs varied in different extraction methods. Furthermore, 13 phenolic compounds in PPPs, including rutin, myricitrin, myricetin, quercetin, kaempferol, protocatechuic acid, gallocatechin, p-hydroxybenzoic acid, ampelopsin, quercetin-7,4′-diglucoside, dihydroquercetin, 5-methylmyricetin, and naringenin, were identified. The relatively strong in vitro antioxidant activities, antiglycation effects, and inhibition activities on α-glucosidase and α-amylase were determined in both PPP-W and PPP-P obtained by HWE and PWE, respectively. The high content of total polyphenolics may be one of the main contributors to their in vitro bioactivities. The findings have shown that the PWE method can be an appropriate method to prepare PPPs with strong bioactivities for application in the functional food industry.
Methods for detecting circulating microRNAs (miRNAs), small RNAs that control gene expression, at high sensitivity and specificity in the blood have been reported in recent studies. The goal of this study was to determine if detectable levels of specific miRNAs are released into the circulation for bevacizumab-induced cardiotoxicity. A miRNA array analysis was performed using RNA isolated from 10 control patients in bevacizumab treatment, and n=10 patients have been confirmed to have bevacizumab-induced cardiotoxicity. From the array, we selected 19 candidate miRNA for a second validation study in 90 controls and 88 patients with bevacizumab-induced cardiotoxicity. Consistent with the data obtained from the microRNA array, circulating levels of five miRNAs were significantly increased in patients with bevacizumab-induced cardiotoxicity compared with controls. To confirm these data, we compared selected miRNAs in the plasma of patients with bevacizumab-induced cardiotoxicity with those of 66 patients with acute myocardial infarction (AMI). Moreover, we went on to analyze what factors may influence the levels of potential biomarker miRNAs. Consistent with the data obtained from the microRNA array, circulating levels of five miRNAs were significantly increased in patients with bevacizumab-induced cardiotoxicity compared with those of healthy bevacizumab treatment controls. However, only miRNA1254 and miRNA579 showed high specificity in the validation experiments. Moreover, we went on to analyze what factors may influence the levels of potential biomarker miRNAs. We identify two miRNAs that are specifically elevated in patients with bevacizumab-induced cardiotoxicity, miR1254 and miRNA579, and miRNA1254 shows the strongest correlation to the clinical diagnosis of bevacizumab-induced cardiotoxicity.
Percutaneous coronary intervention for coronary artery disease treatment often results in pathological vascular injury, characterized by P‐selectin overexpression. Adipose‐derived stem cells (ADSCs) therapeutic efficacy remains elusive due to poor ADSCs targeting and retention in injured vessels. Here, conjugated P‐selectin binding peptide (PBP) to polyethylene glycol‐conjugated phospholipid derivative (DMPE‐PEG) linkers (DMPE‐PEG‐PBP; DPP) are used to facilitate the modification of PBP onto ADSCs cell surfaces via hydrophobic interactions between DMPE‐PEG and the phospholipid bilayer. DPP modification neither has influence on ADSCs proliferation nor apoptosis/paracrine factor gene expression. A total of 5 × 10−6 m DPP‐modified ADSCs (DPP‐ADSCs) strongly binds to P‐selectin‐displaying activated platelets and endothelial cells (ECs) in vitro and to wire‐injured rat femoral arteries when administered by intra‐arterial injection. Targeted binding of ADSCs shields injury sites from platelet and leukocyte adhesion, thereby decreasing inflammation at injury sites. Furthermore, targeted binding of ADSCs recovers injured ECs functionality and reduces platelet‐initiated vascular smooth muscle cells (VSMCs) chemotactic migration. Targeted binding of DPP‐human ADSCs to balloon‐injured human femoral arteries is also demonstrated in ex vivo experiments. Overall, DPP‐ADSCs promote vascular repair, inhibit neointimal hyperplasia, increase endothelium functionality, and maintain normal VSMCs alignment, supporting preclinical noninvasive utilization of DPP‐ADSCs for vascular injury.
Designing hydrogel-based constructs capable of adjusting immune cell functions holds promise for skin tissue regeneration. Mesenchymal stem cell (MSC)-derived small extracellular vesicles (sEVs) have attracted increasing attention owing to their anti-inflammatory and proangiogenic effects. Herein, we constructed a biofunctional hydrogel in which MSC-derived sEVs were incorporated into the injectable hyaluronic acid (HA) hydrogel, thus endowing the hydrogel with immunomodulatory effects. When implanted onto the wound site in a mouse large skin injury model, this functional hydrogel facilitates wound healing and inhibits scar tissue formation by driving macrophages towards an anti-inflammatory and anti-fibrotic (M2c) phenotype. Further investigation showed that the M2c-like phenotype induced by MSC-derived sEVs markedly inhibited the activation of fibroblasts, which could result in scarless skin wound healing. Taken together, these results suggest that modulation of the immune response is a promising and efficient approach to prevent fibrotic scar formation.
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