tretinoin has been researched along with Wounds-and-Injuries* in 8 studies
1 review(s) available for tretinoin and Wounds-and-Injuries
1 trial(s) available for tretinoin and Wounds-and-Injuries
7 other study(ies) available for tretinoin and Wounds-and-Injuries
Article | Year |
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Role of TLR5 in the Translocation and Dissemination of Commensal Bacteria in the Intestine after Traumatic Hemorrhagic Shock.
Enterogenous infection is a major cause of death during traumatic hemorrhagic shock (THS). It has been reported that Toll-like receptor 5 (TLR5) plays an integral role in regulating mucosal immunity and intestinal homeostasis of the microbiota. However, the roles played by TLR5 on intestinal barrier maintenance and commensal bacterial translocation post-THS are poorly understood. In this research, we established THS models in wild-type (WT) and Topics: Animals; Cell Differentiation; Dendritic Cells; Humans; Immunity, Mucosal; Intestines; Lymphocyte Activation; Mice; Mice, Inbred C57BL; Mice, Knockout; Mucous Membrane; Shock, Hemorrhagic; Symbiosis; Th1 Cells; Toll-Like Receptor 5; Tretinoin; Wounds and Injuries | 2021 |
Effects of tretinoin on wound healing in aged skin.
Aged and adult populations have differences in the structural, biological, and healing properties of skin. Comparative studies of healing under the influence of retinoids in both these populations are very important and, to the best of our knowledge, have not been performed to date. The purpose of this study was to compare the activities of topical tretinoin in aged and adult animal models of wound healing by secondary intention. Male aged rats (24 months old, n = 7) and adult rats (6 months old, n = 8) were used. The rats were assigned to the following groups according to the dates on which wound samples were excised (day 14 or 21 after model creation): treated group, control group, and naive group. Topical application of tretinoin cream was used only on the proximal wound and was applied daily for 7 days. Wound healing areas were measured using metal calipers, and morphological analysis was performed. Slides were stained with Hematoxylin and Eosin, Masson's trichrome, and periodic acid-Schiff stains. Statistical analysis adopted a 5% coefficient for rejection of the null hypothesis. Although aged animals showed skin repair, complete reepithelialization was found on day 21 in some animals of both groups (treated and control). In aged rats, the wound area was significantly smaller in treated wounds than in untreated wounds, resulting in a larger scar area compared with the adult group. When treated wounds were compared, no differences were found between the wound areas in adult and aged rats. As expected, the collagen concentration was higher in normal skin from adult rats than in normal skin from aged animals, but there was no difference when aged skin was treated with tretinoin. These results indicate that tretinoin increases collagen synthesis in aged skin and returns the healing process to a normal state of skin healing. Topics: Animals; Collagen; Disease Models, Animal; Granulation Tissue; Keratolytic Agents; Male; Rats; Rats, Wistar; Re-Epithelialization; Skin Aging; Tretinoin; Wound Healing; Wounds and Injuries | 2016 |
Effects of hyperbaric oxygen treatment on antimicrobial function and apoptosis of differentiated HL-60 (neutrophil-like) cells.
Neutrophil apoptosis is important in the resolution of inflammation in chronic wounds. Hyperbaric oxygen (HBO) therapy, an intermittent inhalation of 100% oxygen at greater than atmospheric pressure, appears to be an effective treatment for chronic wounds. The aim was to use HL-60 cells differentiated using all-trans retinoic acid (ATRA) (neutrophil-like cells) to test the hypothesis that an HBO-induced increase in antimicrobial activity might lead to an increase in apoptosis, thereby contributing to neutrophil clearance from chronic wounds.. ATRA differentiated HL-60 cells, an in vitro neutrophil model, were used to test the effects of normoxia, hypoxia (5% O2), hyperoxia (95% O2), hyperbaric normoxia (pressure) (8.8% O2 at 2.4 ATA) and HBO (97.9% O2 at 2.4 ATA) on antimicrobial function [NBT staining, superoxide and H2O2 production, and phagocytosis activity] and apoptosis (caspase 3/7 activity and morphological changes observed using SYBR Safe staining).. A single 90min HBO exposure caused an increase in the respiratory burst activity of neutrophil-like cells post exposure. Phagocytosis of Staphylococcus aureus was also increased. HBO pre-treatment had a pro-apoptotic effect, increasing caspase 3/7 activity and causing morphological changes associated with apoptosis.. The potential detrimental effect of enhanced antimicrobial activity induced by HBO may be offset by enhanced apoptosis. Both hyperoxia and pressure alone seemed to contribute to the HBO-induced increases in antimicrobial activity and apoptosis, although there was no consistent pattern. These data contribute to explaining the effectiveness of HBO in the treatment of chronic wounds. Topics: Apoptosis; Caspase 3; Caspase 7; Cell Death; Cell Differentiation; HL-60 Cells; Humans; Hydrogen Peroxide; Hyperbaric Oxygenation; Neutrophils; Phagocytosis; Staphylococcus aureus; Superoxides; Tretinoin; Wounds and Injuries | 2013 |
The effects of retinoids on secondary wound healing: biometrical and histopathological study in rats.
A wound healing is a complex process, and the role of retinoids in this process is debated and controversial. In this study, the effect of topical tretinoin and oral acitretin on wound healing process was investigated in full-thickness skin lesions on rat model.. A circular full-thickness wound was created by 6 mm punch biopsy on the back side of 32 male rats. The rats were seperated into four equal. The first group was assigned as a control group and was observed with no treatment. The second group was administered dexpanthenol once a day over wound area. In the third group, 0.1% tretinoin cream was applied daily. In the fourth group, 2.5 mg/kg/day acitretin was given daily. Additionally, the biopsies were taken from wounds for the histopathologic examination.. The complete recovery time was remarkably longer in the tretionin group than the control group and the dexpantenol group (p < 0.05). The average complete recovery time was significantly longer in the acitretin group than the control and dexpanthenol groups whereas it was statistically shorter in the acitrein group than the tretionin group (p < 0.05).. Based on our findings, topical tretinoin and oral acitretin can delay secondary wound healing, epithelization and angiogenesis. Topics: Acitretin; Administration, Oral; Administration, Topical; Animals; Keratolytic Agents; Male; Neovascularization, Physiologic; Rats; Rats, Sprague-Dawley; Re-Epithelialization; Skin; Time Factors; Tretinoin; Wound Healing; Wounds and Injuries | 2013 |
Gene expression monitoring for gene discovery in models of peripheral and central nervous system differentiation, regeneration, and trauma.
Gene expression monitoring using gene expression microarrays represents an extremely powerful technology for gene discovery in a variety of systems. We describe the results of seven experiments using Incyte GEM technology to compile a proprietary portfolio of data concerning differential gene expression in six different models of neuronal differentiation and regeneration, and recovery from injury or disease. Our first two experiments cataloged genes significantly up- or down-regulated during two phases of the retinoic acid-induced differentiation of the embryonal carcinoma line Ntera-2. To identify genes involved in neuronal regeneration we performed three GEM experiments, which included changes in gene expression in rat dorsal root ganglia during the healing of experimentally injured sciatic nerve, in regenerating neonatal opossum spinal cord, and during lipopolysaccharide stimulation of primary cultures of rat Schwann cells. Finally we have monitored genes involved in the recovery phase of the inflammatory disease of the rat spinal cord, experimental allergic encephalomyelitis, as well as those responsible for protection from oxidative stress in a glutamate-resistant rat hippocampal cell line. Analysis of the results of the approximately 70,000 data points collected is presented. Topics: Animals; Cell Differentiation; Central Nervous System; Female; Gene Expression Profiling; Lipopolysaccharides; Rats; Rats, Inbred Lew; Rats, Sprague-Dawley; RNA, Messenger; Schwann Cells; Tretinoin; Tumor Cells, Cultured; Wounds and Injuries | 2000 |
Altered wound arginine metabolism by corticosterone and retinoic acid.
Arginine metabolism plays an important role in many aspects of inflammation and wound healing. In this study, we tested the hypothesis that steroids and vitamin A have differential effects on arginine metabolism and thereby may provide a mechanism by which steroids impair wound healing, and vitamin A improves this impairment. Rats were treated with subcutaneous corticosterone pellets 2 days prior to wounding. Intraperitoneal injections of all-trans retinoic acid in peanut oil were administered at the same time and repeated 2 and 4 days later. Polyvinyl alcohol sponges were implanted subcutaneously through a dorsal incision. On Postwounding Days 1, 5, 10, and 15, wound fluid was recovered from the sponges and assayed for nitrite/nitrate (NOx), citrulline, arginine, and ornithine concentrations as well as arginase activity. Steroid treatment decreased the metabolism of arginine to nitric oxide in the early phase of wound healing, and retinoic acid did not change this relationship. Corticosterone also decreased metabolism of arginine to ornithine in the later wound. This depression was inhibited by concomitant administration of retinoic acid. Considering the importance of nitric oxide in host defense and ornithine as a precursor for polyamine and proline synthesis, these data provide a mechanism by which vitamin A improves wound strength, but does not improve wound infection rates in steroid-treated animals. Topics: Animals; Arginase; Arginine; Citrulline; Corticosterone; Male; Nitric Oxide; Nitric Oxide Synthase; Ornithine; Rats; Rats, Sprague-Dawley; Tretinoin; Wound Healing; Wounds and Injuries | 1997 |
Tumor necrosis factor alpha and interleukin 1 alpha induce anchorage independence in v-jun transgenic murine cells.
The oncogene jun encodes a transcription factor of the AP-1 family. In mice carrying viral jun (v-jun) as a transgene, wounding is a prerequisite for tumorigenesis, suggesting collaboration between the transgene and a wound-related event. To define possible candidates for this collaborative process, we examined the effect of several wound-related polypeptide growth factors on cells from transgenic mice. Tumor necrosis factor alpha and interleukin 1 alpha induce anchorage independence in embryo fibroblasts and tumor cell revertants from these mice. This effect was specific for the two cytokines and was restricted to cells from v-jun transgenic mice. Anchorage independence required the continued presence of the cytokines. Transfection of transgenic cells with a v-jun expression plasmid also induced anchorage independence and a tumorigenic phenotype in transgenic tumor cell revertants. However, there was no correlation between anchorage independence, expression of Jun, and AP-1 activity. These results suggest that while increased transgene expression can enhance the growth properties of v-jun transgenic cells, there exist other cytokine-dependent mechanisms that have a similar effect. Retinoic acid, dexamethasone, or forskolin inhibits induction of anchorage independence by tumor necrosis factor alpha, interleukin 1 alpha, and transfected v-jun. Although these agents affect both AP-1 transactivation potential and DNA binding in the transgenic cells, the changes are not correlated with the inhibition of growth. Topics: Animals; Cell Adhesion; Cell Division; Cell Line; Cell Transformation, Neoplastic; Colforsin; Dexamethasone; Embryo, Mammalian; Fibroblasts; Gene Expression; Genes, jun; Growth Substances; Interleukin-1; Mice; Mice, Inbred C57BL; Mice, Transgenic; Sarcoma, Experimental; Sensitivity and Specificity; Stimulation, Chemical; Transcription, Genetic; Transforming Growth Factor alpha; Tretinoin; Wounds and Injuries | 1993 |