Injured Tissue Research Articles

Wet Tissue Interfacial Water Triggers Ultrafast In Situ Gelation of Sprayable Dry Powder for Postoperative Anti‐Adhesion

AbstractPostoperative adhesions complicate the majority of surgical procedures, imposing an excess medical burden. The segregation of injured tissue from healthy tissue is considered the optimal therapeutic strategy. However, achieving hemostasis while preventing adhesions in the immediate postoperative setting continues to pose a significant challenge. This paper presents the in situ formation of an asymmetrically adhesive hydrogel barrier via a sprayable dry powder (SDP) that enables interfacial water‐induced, ultra‐rapid gelation. Owing to SDP hydrophilicity and the interstitial spaces between particles, it can rapidly and efficiently absorb interfacial water, thereby facilitating smooth cross‐linking between material functional groups and tissue functional groups. In addition, SDP becomes less adhesive after gelation as a layer of interfacial water forms on the surface of the SDP hydrogel, enhancing its anti‐adhesion properties. Animal experiment outcomes demonstrate that SDP exhibits significant asymmetric adhesive properties before and after gelation, successfully preventing postoperative adhesions. As a result, SDP heralds a novel approach to the development of adhesives that can simultaneously mitigate adhesions and promptly arrest bleeding.

Preparation and characterization of amidated pectin-gelatin-oxidized tannic acid hydrogel films supplemented with in-situ reduced silver nanoparticles for wound-dressing applications

Wound dressings play a crucial role in protecting injured tissues and promoting the healing process. Traditional fabrication of antibacterial wound dressings can be complex and may involve toxic components. In this study, we developed an innovative hydrogel film (AP:GE@OTA/Ag) composed of amidated pectin (AP), gelatin (GE), oxidized tannic acid (OTA) at varying concentrations, and in-situ reduced silver nanoparticles (AgNPs). FTIR and XRD analyses confirmed that crosslinking occurs via interactions between OTA quinone groups and free amino groups in AP and GE. TEM imaging demonstrated the well-dispersed AgNPs with an average particle size of 58.64 nm, while the TG measurements indicated the enhancement of the thermal stability compared to AP:GE films. The AP:GE@OTA/Ag films exhibited superior fluid uptake ability (90.96 % at 2 h), water retention capacity (91.69 % at 2 h), and water vapor transmission rate (1903.29 g/m2/day), alongside improved tensile strength (38 MPa). Additionally, these films showed excellent cytocompatibility and sustained potent antimicrobial activity against S. aureus and E. coli with low AgNPs loadings of 1.02 ± 0.13 μg/cm2. NIT-1 mouse insulinoma cells demonstrated robust proliferation when cultured with the prepared dressings. These films significantly accelerated wound repair in a skin excision model, indicating their potential clinical applications for wound healing.

Antagonistic activities of endophytic fungi isolated from pines against Diplodia sapinea (Fr.) Fuckel

Diplodia sapinea, an endophytic fungus belonging to the Ascomycota, is commonly found on coniferous trees. While it typically exists as an endophyte, it can transform into an opportunistic pathogen under abiotic stress factors such as drought induced by climate change. The fungus enters the host through stomata on needles or via injured tissues, causing a disease known as Diplodia tip blight. This disease affects trees in various environments, including nurseries, plantation areas, natural forests, and urban trees. The prevalence of D. sapinea has significantly increased in Europe in recent years, and there is currently no established and effective control method worldwide. In response to this challenge, biological control method utilizing antagonist organisms have emerged as a promising alternative to combat Diplodia tip blight. The objective of this study is to evaluate the antagonistic activities of endophytic fungi isolated from different pine tree tissues against D. sapinea isolates obtained from Pinus halepensis and Pinus brutia under in vitro conditions. Identification of the isolates was carried out using both morphological and molecular methods. Fungal inhibition tests were conducted to assess the interaction between these isolates and D. sapinea isolates. The results of the tests revealed that 15 fungi, including Trichoderma sp. and Sydowia polyspora, demonstrated the potential to inhibit the growth of D. sapinea in vitro.

Distinct phenotypes induced by acute hypoxia and TGF-β1 in human adult cardiac fibroblasts

Myocardial infarction (MI) causes hypoxic injury to downstream myocardial tissue, which initiates a wound healing response that replaces injured myocardial tissue with a scar. Wound healing is a complex process that consists of multiple phases, in which many different stimuli induce cardiac fibroblasts to differentiate into myofibroblasts and deposit new matrix. While this process is necessary to replace necrotic tissue, excessive and unresolved fibrosis is common post-MI and correlated with heart failure. Therefore, defining how cardiac fibroblast phenotypes are distinctly regulated by stimuli that are prevalent in the post-MI microenvironment, such as hypoxia and transforming growth factor-beta (TGF-β), is essential for understanding and ultimately mitigating pathological fibrosis. In this study, we acutely treated primary human adult cardiac fibroblasts with TGF-β1 or hypoxia and then characterized their phenotype through immunofluorescence, quantitative RT-PCR, and proteomic analysis. We found that fibroblasts responded to low oxygen with increased localization of hypoxia inducible factor 1 (HIF-1) to the nuclei after 4 h, which was followed by increased gene expression of vascular endothelial growth factor A (VEGFA), a known target of HIF-1, by 24 h. Both TGF-β1 and hypoxia inhibited proliferation after 24 h. TGF-β1 treatment also upregulated various fibrotic pathways. In contrast, hypoxia caused a reduction in several protein synthesis pathways, including collagen biosynthesis. Collectively, these data suggest that TGF-β1, but not acute hypoxia, robustly induces the differentiation of human cardiac fibroblasts into myofibroblasts. Discerning the overlapping and distinctive outcomes of TGF-β1 and hypoxia treatment is important for elucidating their roles in fibrotic remodeling post-MI and provides insight into potential therapeutic targets.

Does The Scientific Evidence Support the Idea of Promoting Sucralfate as The First Aid Topical Management for Burn Wound? A Literature Review

Burn injuries, caused by heat, chemicals, radiation, or electricity, significantly impact morbidity and mortality. Sucralfate, a mucoprotective agent composed of sucrose sulfate and aluminum hydroxide, forms a protective barrier on wounds, reduces pain, stimulates healing, and has anti-inflammatory effects. By stimulating prostaglandin secretion and binding to proteins in the ulcer bed, sucralfate enhances gastrointestinal mucosa defenses and acts locally in injured tissues, minimizing systemic effects. Clinical studies demonstrate its effectiveness in improving wound healing, reducing pain, and promoting tissue regeneration, angiogenesis, and granulation tissue development in burn patients. For optimal burn wound therapy, proper patient selection, formulation techniques, and integration with standard protocols are crucial. Further large-scale randomized controlled trials are necessary to establish guidelines and expand sucralfate's clinical applications.

Old age alters inflammation and autophagy signaling in the brain, leading to exacerbated neurological outcomes after spinal cord injury in male mice

Older patients with spinal cord injury (SCI) have different features with regard to neurological characteristics after injury. Recent large-scale longitudinal population-based studies showed that individuals with SCI are at a higher risk of developing dementia than non-SCI patients, indicating that SCI is a potential risk factor for dementia. Aging is known to potentiate inflammation and neurodegeneration at the injured site leading to impaired recovery from SCI. However, no research has been aimed at studying the mechanisms of SCI-mediated cognitive impairment in the elderly. The present study examined neurobehavioral and molecular changes in the brain and the underlying mechanisms associated with brain dysfunction in aged C57BL/6 male mice using a contusion SCI model. At 2 months post-injury, aged mice displayed worse performance in locomotor, cognitive and depressive-like behavioral tests compared to young adult animals. Histopathology in injured spinal cord tissue was exacerbated in aged SCI mice. In the brain, transcriptomic analysis with NanoString neuropathology panel identified activated microglia and dysregulated autophagy as the most significantly altered pathways by both age and injury. These findings were further validated by flow cytometry, which demonstrated increased myeloid and lymphocytes infiltration at both the injured site and brain of aged mice. Moreover, SCI in aged mice altered microglial function and dysregulated autophagy in microglia, resulting in worsened neurodegeneration. Taken together, our data indicate that old age exacerbates neuropathological changes in both the injured spinal cord and remote brain regions leading to poorer functional outcomes, at least in part, through altered inflammation and autophagy function.

Transcriptional profiling of lung macrophages following ozone exposure in mice identifies signaling pathways regulating immunometabolic activation.

Macrophages play a key role in ozone-induced lung injury by regulating both the initiation and resolution of inflammation. These distinct activities are mediated by pro-inflammatory and anti-inflammatory/proresolution macrophages which sequentially accumulate in injured tissues. Macrophage activation is dependent, in part, on intracellular metabolism. Herein, we used RNA-sequencing (seq) to identify signaling pathways regulating macrophage immunometabolic activity following exposure of mice to ozone (0.8 ppm, 3 h) or air control. Analysis of lung macrophages using an Agilent Seahorse showed that inhalation of ozone increased macrophage glycolytic activity and oxidative phosphorylation at 24 and 72 h post-exposure. An increase in the percentage of macrophages in S phase of the cell cycle was observed 24 h post ozone. RNA-seq revealed significant enrichment of pathways involved in innate immune signaling and cytokine production among differentially expressed genes at both 24 and 72 h after ozone, whereas pathways involved in cell cycle regulation were upregulated at 24 h and intracellular metabolism at 72 h. An interaction network analysis identified tumor suppressor 53 (TP53), E2F family of transcription factors (E2Fs), cyclin-dependent kinase inhibitor 1A (CDKN1a/p21), and cyclin D1 (CCND1) as upstream regulators of cell cycle pathways at 24 h and TP53, nuclear receptor subfamily 4 group a member 1 (NR4A1/Nur77), and estrogen receptor alpha (ESR1/ERα) as central upstream regulators of mitochondrial respiration pathways at 72 h. To assess whether ERα regulates metabolic activity, we used ERα-/- mice. In both air and ozone-exposed mice, loss of ERα resulted in increases in glycolytic capacity and glycolytic reserve in lung macrophages with no effect on mitochondrial oxidative phosphorylation. Taken together, these results highlight the complex interaction between cell cycle, intracellular metabolism, and macrophage activation which may be important in the initiation and resolution of inflammation following ozone exposure.

The TRIM28/miR133a/CD47 axis acts as a potential therapeutic target in pancreatic necrosis by impairing efferocytosis

Efferocytosis, the clearance of apoptotic cells by macrophages, plays a crucial role in inflammatory responses and effectively prevents secondary necrosis. However, the mechanisms underlying efferocytosis in acute pancreatitis (AP) remain unclear. In this study, we demonstrated the presence of efferocytosis in injured human and mouse pancreatic tissues. We also observed significant upregulation of CD47, an efferocytosis-related the "do not eat me" molecule in injured acinar cells. Subsequently, we used CRISPR-Cas9 gene editing, anti-adeno-associated virus (AAV) gene modification, and anti-CD47 antibody to investigate the potential therapeutic role of AP. CD47 expression was negatively regulated by upstream miR133a, which is controlled by the transcription factor TRIM28. To further investigate the regulation of efferocytosis and reduction of pancreatic necrosis in AP, we used miR-133a-agomir and pancreas-specific AAV-shTRIM28 to modulate CD47 expression. Our findings confirmed that CD47-mediated efferocytosis is critical for preventing pancreatic necrosis and suggest that targeting the TRIM28-miR133a-CD47 axis is clinically relevant for the treatment of AP.

Nephrectomy for emphysematous pyelonephritis in a nonfunctional renal allograft due to rejection after kidney transplantation

BackgroundEmphysematous pyelonephritis represents an acute and necrotizing infection characterized by the accumulation of gas within the kidney. This condition poses a swift progression toward sepsis, leading to a poor prognosis. We experienced a rare case of emphysematous pyelonephritis in a nonfunctioning renal allograft attributed to antibody‐mediated rejection after kidney transplantation.Case presentationA 71-year-old man with diabetes had undergone living-donor renal transplantation from his wife. Unfortunately, the transplanted kidney’s function declined due to antibody-mediated rejection, necessitating the introduction of hemodialysis 12 months post-transplantation. Subsequently, 4 months after initiating hemodialysis, the patient presented with pain and swelling in the right lower abdomen. A computed tomography scan revealed the enlargement of the transplanted kidney and gas formation. This constellation of symptoms led to the diagnosis of emphysematous pyelonephritis, resulting in his hospitalization. Further contrast-enhanced computed tomography scans demonstrated an absence of arterial flow and ischemia within the renal allograft. Despite antibiotic treatment and percutaneous drainage, both the gas and fluid in the renal parenchyma and surrounding tissue displayed minimal reduction. Given these compelling findings, an allograft nephrectomy was performed 20 days into his hospital stay. Pathological examination confirmed complete allograft necrosis, revealing nonviable renal parenchyma. The patient’s postoperative recovery progressed favorably.ConclusionsInstances of emphysematous pyelonephritis within transplanted kidneys are infrequently documented. Among these cases, emphysematous pyelonephritis in a nonfunctioning renal allograft is very rare and may be associated with graft ischemia and the presence of injured tissue. The determination of an immediate diagnosis and surgery is important.

Fullerol-reinforced antioxidantive 3D-printed bredigite scaffold for accelerating bone healing

Reactive oxygen species play a vital role in tissue repair, and nonequilibrium of redox homeostasis around bone defect can compromise osteogenesis. However, insufficient antioxidant capacity and weak osteogenic performance remain major obstacles for bone scaffold materials. Herein, integrating the mussel-inspired polydopamine (PDA) coating and 3D printing technologies, we utilized the merits of both osteogenic bredigite and antioxidative fullerol to construct 3D-printed porous, biodegradable acid-buffering, reactive oxygen species (ROS) -scavenging and robust osteogenic bio-scaffold (denoted “FPBS”) for in situ bone defect restoration under oxidative stress microenvironment. Initially, fullerol nanoparticles were attached to the surface of the bredigite scaffold via covalently inter-crosslinking with PDA. Upon injury, extracellular ROS capturing triggered the oxidative degradation of PDA, releasing fullerol nanoparticles to enter into cells for further intracellular ROS scavenging. In vitro, FPBS had good biocompatibility and excellent antioxidative capability. Furthermore, FPBS promoted the osteogenesis of stem cells with significant elevation of osteogenic markers. Finally, in vivo implantation of FPBS remarkably enhanced new bone formation in a rat critical calvarial defect model. Overall, with amelioration of the ROS microenvironment of injured tissue and enhancement of osteogenic differentiation of stem cells simultaneously, FPBS may hold great potential towards bone defect repair.

CD36 deletion prevents white matter injury by modulating microglia polarization through the Traf5-MAPK signal pathway

BackgroundWhite matter injury (WMI) represents a significant etiological factor contributing to neurological impairment subsequent to Traumatic Brain Injury (TBI). CD36 receptors are recognized as pivotal participants in the pathogenesis of neurological disorders, including stroke and spinal cord injury. Furthermore, dynamic fluctuations in the phenotypic polarization of microglial cells have been intimately associated with the regenerative processes within the injured tissue following TBI. Nevertheless, there is a paucity of research addressing the impact of CD36 receptors on WMI and microglial polarization. This investigation aims to elucidate the functional role and mechanistic underpinnings of CD36 in modulating microglial polarization and WMI following TBI.MethodsTBI models were induced in murine subjects via controlled cortical impact (CCI). The spatiotemporal patterns of CD36 expression were examined through quantitative polymerase chain reaction (qPCR), Western blot analysis, and immunofluorescence staining. The extent of white matter injury was assessed via transmission electron microscopy, Luxol Fast Blue (LFB) staining, and immunofluorescence staining. Transcriptome sequencing was employed to dissect the molecular mechanisms underlying CD36 down-regulation and its influence on white matter damage. Microglial polarization status was ascertained using qPCR, Western blot analysis, and immunofluorescence staining. In vitro, a Transwell co-culture system was employed to investigate the impact of CD36-dependent microglial polarization on oligodendrocytes subjected to oxygen-glucose deprivation (OGD).ResultsWestern blot and qPCR analyses revealed that CD36 expression reached its zenith at 7 days post-TBI and remained sustained at this level thereafter. Immunofluorescence staining exhibited robust CD36 expression in astrocytes and microglia following TBI. Genetic deletion of CD36 ameliorated TBI-induced white matter injury, as evidenced by a reduced SMI-32/MBP ratio and G-ratio. Transcriptome sequencing unveiled differentially expressed genes enriched in processes linked to microglial activation, regulation of neuroinflammation, and the TNF signaling pathway. Additionally, bioinformatics analysis pinpointed the Traf5-p38 axis as a critical signaling pathway. In vivo and in vitro experiments indicated that inhibition of the CD36-Traf5-MAPK axis curtailed microglial polarization toward the pro-inflammatory phenotype. In a Transwell co-culture system, BV2 cells treated with LPS + IFN-γ exacerbated the damage of post-OGD oligodendrocytes, which could be rectified through CD36 knockdown in BV2 cells.ConclusionsThis study illuminates that the suppression of CD36 mitigates WMI by constraining microglial polarization towards the pro-inflammatory phenotype through the down-regulation of the Traf5-MAPK signaling pathway. Our findings present a potential therapeutic strategy for averting neuroinflammatory responses and ensuing WMI damage resulting from TBI.Graphical

G protein subunit Gγ13-mediated signaling pathway is critical to the inflammation resolution and functional recovery of severely injured lungs.

Tuft cells are a group of rare epithelial cells that can detect pathogenic microbes and parasites. Many of these cells express signaling proteins initially found in taste buds. It is, however, not well understood how these taste signaling proteins contribute to the response to the invading pathogens or to the recovery of injured tissues. In this study, we conditionally nullified the signaling G protein subunit Gγ13 and found that the number of ectopic tuft cells in the injured lung was reduced following the infection of the influenza virus H1N1. Furthermore, the infected mutant mice exhibited significantly larger areas of lung injury, increased macrophage infiltration, severer pulmonary epithelial leakage, augmented pyroptosis and cell death, greater bodyweight loss, slower recovery, worsened fibrosis and increased fatality. Our data demonstrate that the Gγ13-mediated signal transduction pathway is critical to tuft cells-mediated inflammation resolution and functional repair of the damaged lungs.To our best knowledge, it is the first report indicating subtype-specific contributions of tuft cells to the resolution and recovery.

G protein subunit Gγ13-mediated signaling pathway is critical to the inflammation resolution and functional recovery of severely injured lungs

Tuft cells are a group of rare epithelial cells that can detect pathogenic microbes and parasites. Many of these cells express signaling proteins initially found in taste buds. It is, however, not well understood how these taste signaling proteins contribute to the response to the invading pathogens or to the recovery of injured tissues. In this study, we conditionally nullified the signaling G protein subunit Gγ13 and found that the number of ectopic tuft cells in the injured lung was reduced following the infection of the influenza virus H1N1. Furthermore, the infected mutant mice exhibited significantly larger areas of lung injury, increased macrophage infiltration, severer pulmonary epithelial leakage, augmented pyroptosis and cell death, greater bodyweight loss, slower recovery, worsened fibrosis and increased fatality. Our data demonstrate that the Gγ13-mediated signal transduction pathway is critical to tuft cells-mediated inflammation resolution and functional repair of the damaged lungs.To our best knowledge, it is the first report indicating subtype-specific contributions of tuft cells to the resolution and recovery.

Neutrophils, the major players in healing after myocardial infarction

Neutrophils are a type of immune cells with controversial functions. While their role in the protection against the microbial invasion is well known, the role in controlling and monitoring the non-infection healing processes of the injured tissue and organs are now to be discovered. Particularly in the healing after myocardial infarction, the neutrophils were considered for a long time the “bad guys”, sustaining the inflammation and interfering with the repair processes. However, all the attempt to deplete or massively inhibit their activity in experimental conditions or clinical settings lead to catastrophic results, with defective scar formation and worsening of the heart function. As recent studies pointed out the essential role of the neutrophils in monitoring and guiding all the processes involved in the proper tissular healing, a detailed investigation of mechanistic inside is required for a selective and effective design of therapeutical strategies targeting neutrophils to preserve and improve heart function after an acute myocardial infarction.

Modulating Proliferation, Migration and Differentiation of Mesenchymal Stem Cells Using Interleukins

Abstract:: Mesenchymal Stem Cells (MSCs) are multipotent stem cells that are obtained from various tissue sources such as bone marrow, adipose tissues, umbilical cords, dental pulps, and peripheral blood has high regenerative potential, migratory abilities, and immunosuppressive properties. These properties make them attractive candidates for tissue engineering, immunosuppressive therapies, and in vivo drug deliveries. MSCs, because of their high propensity to home in an injured tissue microenvironment, are exposed to various cytokines. These cytokines modulate the activity of MSCs to help in the regeneration of injured tissue. Interleukins are one such cytokine that is present in injured tissue microenvironment and plays significant roles in the activation, differentiation, proliferation, maturation, migration, and adhesion of not only immune cells but also MSCs. Interleukins, through both autocrine and paracrine signaling mechanisms, modulate the functioning of MSCs. This article reviews how interleukins influence MSCs by discussing their signaling pathways, their effect on differentiation and other biological effects. A comprehensive understanding of the influence of interleukins on MSCs may provide insights to manipulate improving the therapeutic potential of MSCs or reducing potential risks such as undesirable immune response and tumor formation.

Emilin2 marks the target region for mesenchymal cell accumulation in bone regeneration

BackgroundRegeneration of injured tissue is dependent on stem/progenitor cells, which can undergo proliferation and maturation processes to replace the lost cells and extracellular matrix (ECM). Bone has a higher regenerative capacity than other tissues, with abundant mesenchymal progenitor cells in the bone marrow, periosteum, and surrounding muscle. However, the treatment of bone fractures is not always successful; a marked number of clinical case reports have described nonunion or delayed healing for various reasons. Supplementation of exogenous stem cells by stem cell therapy is anticipated to improve treatment outcomes; however, there are several drawbacks including the need for special devices for the expansion of stem cells outside the body, low rate of cell viability in the body after transplantation, and oncological complications. The use of endogenous stem/progenitor cells, instead of exogenous cells, would be a possible solution, but it is unclear how these cells migrate towards the injury site.MethodsThe chemoattractant capacity of the elastin microfibril interface located protein 2 (Emilin2), generated by macrophages, was identified by the migration assay and LC–MS/MS. The functions of Emilin2 in bone regeneration were further studied using Emilin2–/– mice.ResultsThe results show that in response to bone injury, there was an increase in Emilin2, an ECM protein. Produced by macrophages, Emilin2 exhibited chemoattractant properties towards mesenchymal cells. Emilin2–/– mice underwent delayed bone regeneration, with a decrease in mesenchymal cells after injury. Local administration of recombinant Emilin2 protein enhanced bone regeneration.ConclusionEmilin2 plays a crucial role in bone regeneration by increasing mesenchymal cells. Therefore, Emilin2 can be used for the treatment of bone fracture by recruiting endogenous progenitor cells.

Macrophages upregulate mural cell-like markers and support healing of ischemic injury by adopting functions important for vascular support

Sterile inflammation after injury is important for tissue restoration. In injured human and mouse tissues, macrophages were recently found to accumulate perivascularly. This study investigates if macrophages adopt a mural cell phenotype important for restoration after ischemic injury. Single-cell RNA sequencing of fate-mapped macrophages from ischemic mouse muscles demonstrates a macrophage-toward-mural cell switch of a subpopulation of macrophages with downregulated myeloid cell genes and upregulated mural cell genes, including PDGFRβ. This observation was further strengthened when including unspliced transcripts in the analysis. The macrophage switch was proven functionally relevant, as induction of macrophage-specific PDGFRβ deficiency prevented their perivascular macrophage phenotype, impaired vessel maturation and increased vessel leakiness, which ultimately reduced limb function. In conclusion, macrophages in adult ischemic tissue were demonstrated to undergo a cellular program to morphologically, transcriptomically and functionally resemble mural cells while weakening their macrophage identity. The macrophage-to-mural cell-like phenotypic switch is crucial for restoring tissue function and warrants further exploration as a potential target for immunotherapies to enhance healing.

Stimuli-responsive Biomaterials for Tissue Engineering Applications.

The use of ''smart materials,'' or ''stimulus responsive'' materials, has proven useful in a variety of fields, including tissue engineering and medication delivery. Many factors, including temperature, pH, redox state, light, and magnetic fields, are being studied for their potential to affect a material's properties, interactions, structure, and/or dimensions. New tissue engineering and drug delivery methods are made possible by the ability of living systems to respond to both external stimuli and their own internal signals) for example, materials composed of stimuliresponsive polymers that self assemble or undergo phase transitions or morphology transformation. The researcher examines the potential of smart materials as controlled drug release vehicles in tissue engineering, aiming to enable the localized regeneration of injured tissue by delivering precisely dosed drugs at precisely timed intervals.

Novel garden cress-fish gelatin based ointment: Improvement of skin wound healing in rats through modulation of anti-inflammatory and antioxidant states

This study aimed to investigate the ability of aqueous extract of Lepidium sativum seeds (LSE) to improve the wound healing process in rat models. The gelatin, extracted from the skin of smooth-hound shark using citric acid, was used as a support material for ointment. Animals were divided into four groups of six rats each: an untreated control group, a control group treated with Moist Exposed Burn Ointment (MEBO), a treated group with gelatin gel, and a treated group with gelatin gel fortified with 20 mg/mL LSE. Phenolics profile analysis showed that the major compounds in LSE were catechin (125 μg/g) and quinic acid (105 μg/g). In vitro antioxidant tests showed that LSE has interesting activities to scavenge ABTS•+ radicals (IC50 = 0.22 mg/mL) and inhibit the oxidation of linoleic acid. A significant decline in the antioxidant enzymes activities and an increase in the level of thiobarbituric acid reactive substances (TBARS) and inflammatory markers was observed within the injured tissues of the untreated rats compared to rats treated with MEBO. Interestingly, when the wounded tissue was treated with gelatin gel a remarkable reversal of this trend occurred. Further, by enrichment of gelatin gel with LSE, the levels of CAT, GPx and SOD activities significantly increased by 35, 126, and 212 %, respectively, whereas the TBARS level was reduced by 31 %. These results were consistent with the wound contraction percentage and histological analysis, which suggest the potential effect of LSE-enriched gelatin gels to regenerate damaged tissues.

Jumps and Plyometric Exercises in the Return to Play After Sports Injuries

Background: Jumps and plyometric exercises represent a fundamental component of high-intensity sports activities and must be included in the return to play programs after a sports injury. However, the scientific literature focused on the prescription methodology of these activities in the return to play programs is limited. Objective: The aim of this manuscript was to provide an overview of the aspects related to the incorporation of jumps and plyometric exercises in the return to play programs. Results: Some clinical criteria that the athlete must meet to be incorporated into jump work and plyometric exercises in return to play programs are capacity of the injured tissue to support the load, absence of symptoms, complete joint mobility, previous acquisition of basic motor patterns of the lower limbs, adequate level of strength and muscular balance and technically consolidated jump gesture. The methodological prescription of jumps and plyometric exercises in return to play programs must consider variables such as the type of jumps, intensity, volume, and execution surface, to guarantee adequate progression and minimize the risk of injury recurrence. Conclusions: Jumps and plyometric exercises are frequently included in intermediate and advanced phases of return to play programs but the information on their prescription in this area is scarce; we establish a methodological guide that can be useful for the prescription of jumps and plyometric exercises in return to play programs, based mainly on biomechanical studies that evaluate various aspects of the joint load during its execution.