scholarly journals Characterization and biological evaluation of a novel silver nanoparticle-loaded collagen-chitosan dressing

2020 ◽  
Vol 7 (4) ◽  
pp. 371-380 ◽  
Author(s):  
Rongfu Li ◽  
Zhaorong Xu ◽  
Qiong Jiang ◽  
Yunquan Zheng ◽  
Zhaohong Chen ◽  
...  

Abstract Effective coverage and protection is a priority in wound treatment. Collagen and chitosan have been widely used for wound dressings due to their excellent biological activity and biocompatibility. Silver nanoparticles (AgNPs) have a powerful antibacterial effect. In this study, a macromolecular and small-molecular collagen mixed solution, a macromolecular and small-molecular chitosan mixed solution were prepared, and a silver nanoparticle-loaded collagen-chitosan dressing (AgNP-CCD) has been proposed. First, the effects of a collagen-chitosan mixed solution on the proliferation of human umbilical vein endothelial cells and the secretion of cytokines were evaluated. Then, the characteristics and antibacterial effects of the AgNP-CCD were tested, and the effects on wound healing and the influence of wound cytokine expression were investigated via a deep second-degree burn wound model. The results showed that at the proper proportion and concentration, the collagen-chitosan mixed solution effectively promoted cell proliferation and regulated the levels of growth factors (vascular endothelial growth factor [VEGF], epidermal growth factor [EGF], platelet-derived growth factor [PDGF], transforming growth factor [TGF-β1], basic fibroblastic growth factor [bFGF]) and inflammatory factors (TNF-α, IL-1β, IL-6, IL-8). Moreover, AgNP solutions at lower concentrations exerted limited inhibitory effects on cell proliferation and had no effect on cytokine secretion. The AgNP-CCD demonstrated satisfactory morphological and physical properties as well as efficient antibacterial activities. An in vivo evaluation indicated that AgNP-CCD could accelerate the healing process of deep second-degree burn wounds and played an important role in the regulation of growth and inflammatory factors, including VEGF, EGFL-7, TGF-β1, bFGF, TNF-α and IL-1β. This AgNP-CCD exerted excellent biological effects on wound healing promotion and cytokine expression regulation.

2002 ◽  
Vol 13 (2) ◽  
pp. 322-331 ◽  
Author(s):  
Youichi Sugenoya ◽  
Ashio Yoshimura ◽  
Hisako Yamamura ◽  
Kiyoko Inui ◽  
Hiroyuki Morita ◽  
...  

ABSTRACT. The basic or h1 calponin gene, which encodes an actin-binding protein involved in the regulation of smooth-muscle shortening velocity, is known to be a smooth-muscle differentiation-specific gene. It was found that basic calponin was expressed by cultured mesangial cells and localized along the actin filaments. Among the growth factors involved in the mesangial cell pathophysiology, including platelet-derived growth factor-BB (PDGF-BB), tumor necrosis factor–α (TNF-α), and transforming growth factor–β1 (TGF-β1), TNF-α potently downregulates basic calponin expression in both the mRNA and protein levels, whereas TGF-β1 upregulates the calponin expression. PDGF-BB also reduced its mRNA expression. The half-life of basic calponin mRNA was determined to be similar between TNF-α–treated and –untreated mesangial cells, whereas cell transfection assays that used a luciferase reporter gene construct containing the functional basic calponin promoter showed that TNF-α and PDGF-BB reduced the transcriptional activity. Because stimulation with TNF-α and PDGF-BB was associated with mesangial cell proliferation, basic calponin may play a role in the suppression of mesangial cell proliferation. Treatment with anti–glomerular basement membrane antibody in calponin knockout mice induced more severe nephritis than in wild type mice, as judged from an increase in the urinary protein excretion, glomerular cellularity, and number of proliferating cell nuclear antigen–positive cells in glomerulus. These results suggest that basic calponin expression may serve as one of the intrinsic regulators of glomerular nephritis. Elucidation of the molecular mechanisms for regulation of the basic calponin expression in mesangial cells may improve the understanding of the molecular basis and pathogenesis of the glomerular response to injury.


2020 ◽  
Author(s):  
Da li Gan ◽  
Yan Yao ◽  
Qi yuan Su ◽  
Su qin Yang ◽  
Li Wu ◽  
...  

Abstract Background: Burn injury is common, burn ointment (BO) is a common preparation used to treat burns and scalds in folk as an effective remedy for burn healing. The present study was undertaken to evaluate the healing effect and related underlying mechanisms of BO in a model of deep second-degree thermal burn by animal experiments. Methods: BO is was made up of a combination of extracts from several traditional Chinese medicine and borneol, solid paraffin, rapeseed oil, and and its quality control was assessed. The acute toxicity test and skin irritation test were evaluated by rats. The anti-inflammatory effect was revealed by using inflammation animal models, including the xylene-induced auricle swelling in mice and carrageenan-induced toe swelling in rats. The hot plate test was used to evaluate its analgesic activity. Moreover, the experiments of knife and a deep second-degree burn wound were used to explore the effect of BO in promoting wound healing. On days 7, 14 and 28, the wounds were digitally photographed by a camera and after sacrifice of the SD rats, skin samples were obtained for performing H&E staining, immunohistochemical staining and Western Blotting examination. In addition, The expressed of TNF-α, TGF-β1 and VEGF in serum were detected by ELISA kits. Results: BO had no toxicity or side effects on the skin and liver or kidney function. BO could significantly inhibit auricular swelling in mice, paw welling in rats and markedly prolonged the latencies of licking paws in mice; it also could accelerate the process of wound healing and repair scar by promoting the formation of new epithelial tissue. In addition, BO significantly reduced the content of TNF-α and markedly increased the content of VEGF and TGF-β1 in the serum. Moreover, BO promoted the expression of collagen I. Furthermore, it increased the ratio of p-PI3K/PI3K, p-AKT/AKT and p-mTOR/mTOR in the PI3K / AKT / mTOR pathway.Conclusions: BO could effectively reduce inflammation and pain, and effectively accelerate the healing process of deep second-degree burn wounds. And the mechanism of BO promoting wound healing may be related to activate PI3K / AKT / mTOR pathway. therefore, it may be recommended as a promising topical medication for treating burn wounds in the future clinical trials.


2021 ◽  
Vol 2021 ◽  
pp. 1-22
Author(s):  
Pouria Rahmanian-Devin ◽  
Hassan Rakhshandeh ◽  
Vafa Baradaran Rahimi ◽  
Zahra Sanei-Far ◽  
Maede Hasanpour ◽  
...  

Postoperative peritoneal adhesions are considered the major complication following abdominal surgeries. The primary clinical complications of peritoneal adhesion are intestinal obstruction, infertility, pelvic pain, and postoperative mortality. In this study, regarding the anti-inflammatory and antioxidant activities of Crocus sativus, we aimed to evaluate the effects of Crocus sativus on the prevention of postsurgical-induced peritoneal adhesion. Male Wistar-Albino rats were used to investigate the preventive effects of C. sativus extract (0.5%, 0.25% and 0.125% w / v ) against postsurgical-induced peritoneal adhesion compared to pirfenidone (PFD, 7.5% w / v ). We also investigated the protective effects of PFD (100 μg/ml) and C. sativus extract (100, 200, and 400 μg/ml) in TGF-β1-induced fibrotic macrophage polarization. The levels of cell proliferation and oxidative, antioxidative, inflammatory and anti-inflammatory, fibrosis, and angiogenesis biomarkers were evaluated both in vivo and in vitro models. C. sativus extract ameliorates postoperational-induced peritoneal adhesion development by attenuating oxidative stress [malondialdehyde (MDA)]; inflammatory mediators [interleukin- (IL-) 6, tumour necrosis factor- (TNF-) α, and prostaglandin E2 (PGE2)]; fibrosis [transforming growth factor- (TGF-) β1, IL-4, and plasminogen activator inhibitor (PAI)]; and angiogenesis [vascular endothelial growth factor (VEGF)] markers, while propagating antioxidant [glutathione (GSH)], anti-inflammatory (IL-10), and fibrinolytic [tissue plasminogen activator (tPA)] markers and tPA/PAI ratio. In a cellular model, we revealed that the extract, without any toxicity, regulated the levels of cell proliferation and inflammatory (TNF-α), angiogenesis (VEGF), anti-inflammatory (IL-10), M1 [inducible nitric oxide synthase (iNOS)] and M2 [arginase-1 (Arg 1)] biomarkers, and iNOS/Arg-1 ratio towards antifibrotic M1 phenotype of macrophage, in a concentration-dependent manner. Taken together, the current study indicated that C. sativus reduces peritoneal adhesion formation by modulating the macrophage polarization from M2 towards M1 cells.


2020 ◽  
Vol 21 (22) ◽  
pp. 8826
Author(s):  
Elena Guillén-Gómez ◽  
Irene Silva ◽  
Núria Serra ◽  
Francisco Caballero ◽  
Jesús Leal ◽  
...  

Pretransplant graft inflammation could be involved in the worse prognosis of deceased donor (DD) kidney transplants. A2A adenosine receptor (A2AR) can stimulate anti-inflammatory M2 macrophages, leading to fibrosis if injury and inflammation persist. Pre-implantation biopsies of kidney donors (47 DD and 21 living donors (LD)) were used to analyze expression levels and activated intracellular pathways related to inflammatory and pro-fibrotic processes. A2AR expression and PKA pathway were enhanced in DD kidneys. A2AR gene expression correlated with TGF-β1 and other profibrotic markers, as well as CD163, C/EBPβ, and Col1A1, which are highly expressed in DD kidneys. TNF-α mRNA levels correlated with profibrotic and anti-inflammatory factors such as TGF-β1 and A2AR. Experiments with THP-1 cells point to the involvement of the TNF-α/NF-κB pathway in the up-regulation of A2AR, which induces the M2 phenotype increasing CD163 and TGF-β1 expression. In DD kidneys, the TNF-α/NF-κB pathway could be involved in the increase of A2AR expression, which would activate the PKA–CREB axis, inducing the macrophage M2 phenotype, TGF-β1 production, and ultimately, fibrosis. Thus, in inflamed DD kidneys, an increase in A2AR expression is associated with the onset of fibrosis, which may contribute to graft dysfunction and prognostic differences between DD and LD transplants.


2021 ◽  
Author(s):  
Liang Qiao ◽  
Rongxia Li ◽  
Shangang Hu ◽  
Yu Liu ◽  
Hongqiang Liu ◽  
...  

Abstract Objective Previously, the protective effect of microRNA (miR)-145-5p has been discovered in acute lung injury (ALI). Thus, this study attempts to further discuss the mechanism of miR-145-5p in ALI through the downstream E26 transformation-specific proto-oncogene 2 (ETS2)/transforming growth factor β1 (TGF-β1)/Smad pathway. Methods A lipopolysaccharide (LPS)-induced rat ALI model was established. Recombinant adenovirus miR-145-5p and/or ETS2 overexpression plasmid was administrated into rats. Afterwards, pathological damage in the lung tissue, wet/dry (W/D) ratio, apoptosis and contents of serum inflammatory factors were observed. miR-145-5p, ETS2, TGF-β1, Smad2/3, phosphorylated Smad2/3 levels were measured in rats. Results miR-145-5p was down-regulated, ETS2 was up-regulated and TGF-β1/Smad pathway was activated in LPS-suffered rats. Overexpression of miR-145-5p inactivated the TGF-β1/Smad pathway and attenuated ALI, as reflected by relived pathological damage, and decreased W/D ratio, apoptosis and inflammatory response. Oppositely, loss of miR-145-5p or enhancement of ETS2 worsened ALI and activated the TGF-β1/Smad pathway. Moreover, elevation of ETS2 decreased miR-145-5p-mediated protection against ALI. Conclusion Evidently, miR-145-5p negatively regulates ETS2 expression and inactivates TGF-β1/Smad pathway to ameliorate ALI in rats.


Polymers ◽  
2021 ◽  
Vol 13 (19) ◽  
pp. 3279
Author(s):  
Longhao Jin ◽  
Sun-Jung Yoon ◽  
Dae Hoon Lee ◽  
Yun Chang Pyun ◽  
Woo Youp Kim ◽  
...  

Wound recovery close to the function of the native skin is the goal of wound healing. In this study, we prepared foam dressings (FDs; 2-GHC-FD-1–9, 5-GHC-FD-1–9, and 10-GHC-FD-1–9) composed of various concentrations of gelatin, hyaluronic acid, and carboxymethyl chitosan, which are chemically interconnected through amide bond formation, for evaluating wound healing. Tensile and cell proliferation tests showed that 2-GHC-FD-1–9 are suitable for wound dressing. For further evaluation, three types of FDs, 2-GHC-FD-1, 2-GHC-FD-4, and 2-GHC-FD-8 were chosen. The results of animal intradermal reactivity, water vapor transmission rate, and absorption rate of the three FDs indicated that 2-GHC-FD-8 is the most appropriate scaffold for wound healing. For wound healing acceleration, various concentrations of fibroblast growth factor-7 (FGF-7) was soaked in 2-GHC-FD-8 (2-GHC-FD-8/F1-6) and evaluated by using scanning electron microscopy, cell proliferation, release behavior, and in vivo animal tests. The FDs showed interconnected porous structures, increased cell proliferation until 8.0 × 10−11 M, controlled release with initial burst within 1 h, and sustained release for 48 h. The results of the animal test showed an appropriate concentration of FGF-7 for wound healing. In addition, 2-GHC-FD-8 is a suitable scaffold for wound healing. Therefore, we suggest that 2-GHC-FD-8/F3 is a useful wound dressing for accelerating wound healing.


2016 ◽  
Vol 40 (1-2) ◽  
pp. 207-218 ◽  
Author(s):  
Zhaohua Jiang ◽  
Qingxiong Yu ◽  
Lingling Xia ◽  
Yi Zhang ◽  
Xiuxia Wang ◽  
...  

Background: Keloids are fibroproliferative scars that develop as a result of a dysregulated wound healing process; however, the molecular mechanisms of keloid pathogenesis remain unclear. Keloids are characterized by the ability to spread beyond the original boundary of the wound, and they represent a significant clinical challenge. Previous work from our group suggested that growth differentiation factor (GDF)-9 plays a role in the invasive behavior of keloids. Here, we examined the involvement of GDF-9 in keloid formation and spread and elucidated a potential underlying mechanism. Methods: The expression of GDF-9, cyclooxygenase (COX)-2, vascular epidermal growth factor (VEGF)-C, matrix metalloprotease (MMP)-2, MMP-9, transforming growth factor (TGF)-β1, and the related signaling pathway components in human keloid tissues or keloid fibroblasts (kFBs) was monitored by qRT-PCR and western blot. A series of overexpression and silencing experiments in normal and keloid fibroblasts were used to modify the expression of GDF-9. The effects of GDF-9 on kFB proliferation and migration were assessed using the CCK-8, cell cycle and scratch wound healing assays. Results: GDF-9 promotes fibroblast proliferation and migration. GDF-9 silencing in kFBs decreased cell proliferation, blocked cell cycle progression, downregulated the angiogenic markers COX-2 and VEGF-C, and downregulated MMP-2 and MMP-9 expression, whereas it had no effect on the levels of TGF-β1. GDF-9 silencing significantly inhibited Smad2 and Smad3 phosphorylation in kFBs. Conclusions: GDF-9 promotes the proliferation and migration of kFBs via a mechanism involving the Smad2/3 pathway.


1998 ◽  
Vol 275 (1) ◽  
pp. L71-L79 ◽  
Author(s):  
Elodie Nabeyrat ◽  
Valérie Besnard ◽  
Sophie Corroyer ◽  
Véronique Cazals ◽  
Annick Clement

Retinoids, including retinol and retinoic acid (RA) derivatives, are important molecules for lung growth and homeostasis. The presence of RA receptors and of RA-binding proteins in the alveolar epithelium led to suggest a role for RA on alveolar epithelial cell replication. In the present study, we examined the effects of RA on proliferation of the stem cells of the alveolar epithelium, the type 2 cells. We showed that treatment of serum-deprived type 2 cells with RA led to a stimulation of cell proliferation, with an increase in cell number in a dose-dependent manner. To gain some insights into the mechanisms involved, we studied the effects of RA on the expression of several components of the insulin-like growth factor (IGF) system that have been shown to be associated with the growth arrest of type 2 cells, mainly the IGF-binding protein-2 (IGFBP-2), IGF-II, and the type 2 IGF receptor. We documented a marked decrease in the expression of these components upon RA treatment. Using conditioned media from RA-treated cells, we provided evidence that the proliferative response of type 2 cells to RA was mediated through production of growth factor(s) distinct from IGF-I. We also showed that RA was able to reduce the decrease in cell number observed when type 2 cells were treated with transforming growth factor (TGF)-β1. These results together with the known stimulatory effect of TGF-β1 on IGFBP-2 expression led to suggest that RA may be associated with type 2 cell proliferation through mechanisms interfering with the TGF-β1 pathway.


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