scholarly journals Nocardia rubra cell wall skeleton accelerates cutaneous wound healing by enhancing macrophage activation and angiogenesis

2018 ◽  
Vol 46 (6) ◽  
pp. 2398-2409 ◽  
Author(s):  
Yi Wang ◽  
Ying Hu ◽  
Ben Ma ◽  
Fei Wang ◽  
Sheng Liu ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cell Wall ◽  
Transforming Growth Factor ◽  
Wound Dressings ◽  
Control Group ◽  
Cutaneous Wound Healing ◽  
Full Thickness ◽  
Cutaneous Wound ◽  
Expression Levels ◽  
Tgf Β1

Objective This study was performed to investigate the effect of Nocardia rubra cell wall skeleton (N-CWS) on wound healing of full-thickness skin defects. Methods Two 2- × 2-cm full-thickness wounds, one on each side of the midline, were made on the back of 12 rats. One wound was covered with Vaseline gauze soaked in normal saline, whereas the other was covered with Vaseline gauze and N-CWS. Wound dressings were changed every other day from day 0 (wound creation) to day 11. Four of the 12 rats were killed on day 7, and biopsy samples were obtained for biochemical and histopathological analyses. The expression levels of CD31, CD68, and F4/80 in the tissues were examined immunohistologically. The expression of transforming growth factor (TGF)-β1 in the wound was determined by western blot. Results N-CWS increased the wound healing rate, reduced the complete wound healing time, and increased the expression levels of CD31, CD68, and F4/80 on day 7. The TGF-β1 expression level in the wound was significantly higher in the N-CWS group than in the control group on day 7. Conclusions N-CWS can activate macrophages, increase TGF-β1 expression, and enhance angiogenesis and thus accelerate cutaneous wound healing.

scholarly journals Collagen extract obtained from Nile tilapia (Oreochromis niloticus L.) skin accelerates wound healing in rat model via up regulating VEGF, bFGF, and α-SMA genes expression

2020 ◽  
Vol 16 (1) ◽  
Author(s):  
Zizy I. Elbialy ◽  
Ayman Atiba ◽  
Aml Abdelnaby ◽  
Ibrahim I. Al-Hawary ◽  
Ahmed Elsheshtawy ◽  
...  
Keyword(s):  
Wound Healing ◽  
Growth Factor ◽  
Rat Model ◽  
Nile Tilapia ◽  
Transforming Growth Factor ◽  
Healing Process ◽  
Control Group ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Genes Expression

Abstract Background Collagen is the most abundant structural protein in the mammalian connective tissue and represents approximately 30% of animal protein. The current study evaluated the potential capacity of collagen extract derived from Nile tilapia skin in improving the cutaneous wound healing in rats and investigated the underlying possible mechanisms. A rat model was used, and the experimental design included a control group (CG) and the tilapia collagen treated group (TCG). Full-thickness wounds were conducted on the back of all the rats under general anesthesia, then the tilapia collagen extract was applied topically on the wound area of TCG. Wound areas of the two experimental groups were measured on days 0, 3, 6, 9, 12, and 15 post-wounding. The stages of the wound granulation tissues were detected by histopathologic examination and the expression of vascular endothelial growth factor (VEGF), and transforming growth factor (TGF-ß1) were investigated using immunohistochemistry. Moreover, relative gene expression analysis of transforming growth factor-beta (TGF-ß1), basic fibroblast growth factor (bFGF), and alpha-smooth muscle actin (α-SMA) were quantified by real-time qPCR. Results The histopathological assessment showed noticeable signs of skin healing in TCG compared to CG. Immunohistochemistry results revealed remarkable enhancement in the expression levels of VEGF and TGF-β1 in TCG. Furthermore, TCG exhibited marked upregulation in the VEGF, bFGF, and α-SMA genes expression. These findings suggested that the topical application of Nile tilapia collagen extract can promote the cutaneous wound healing process in rats, which could be attributed to its stimulating effect on recruiting and activating macrophages to produce chemotactic growth factors, fibroblast proliferation, and angiogenesis. Conclusions The collagen extract could, therefore, be a potential biomaterial for cutaneous wound healing therapeutics.

Study on the Effect of Cerium Oxide Nanocubes on Full-Thickness Cutaneous Wound Healing of Type 2 Diabetic Rats

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 643-P ◽  
Author(s):  
YANFEI HAN ◽  
LINDONG LI ◽  
YANJUN LIU ◽  
YOU WANG ◽  
CHUNHUA YAN ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cerium Oxide ◽  
Diabetic Rats ◽  
Cutaneous Wound Healing ◽  
Full Thickness ◽  
Cutaneous Wound ◽  
Type 2 Diabetic

Estrogen accelerates cutaneous wound healing associated with an increase in TGF-β1 levels

1997 ◽  
Vol 3 (11) ◽  
pp. 1209-1215 ◽  
Author(s):  
Gillian S. Ashcroft ◽  
Joanne Dodsworth ◽  
Egon Van Boxtel ◽  
Roy W. Tarnuzzer ◽  
Michael A. Horan ◽  
...  
Keyword(s):  
Wound Healing ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Tgf Β1

scholarly journals The Effect of 17β-Estradiol Administration on Cutaneous Wound Healing in 24-Week Ovariectomized Female Mice

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Kanae Mukai ◽  
Yukari Nakajima ◽  
Tamae Urai ◽  
Emi Komatsu ◽  
Kana Takata ◽  
...  
Keyword(s):  
Wound Healing ◽  
Inflammatory Response ◽  
Cutaneous Wound Healing ◽  
Full Thickness ◽  
Estrogen Replacement ◽  
Wound Area ◽  
Cutaneous Wound ◽  
Female Mice ◽  
Exogenous Estrogen ◽  
17Β Estradiol

Estrogen replacement promotes cutaneous wound healing in 8–10-week young ovariectomized female mice. However, research using aged ovariectomized female mice has not been reported, to the best of our knowledge. Therefore, we investigated the effect of 17β-estradiol on cutaneous wound healing using 24-week middle-aged ovariectomized female mice. Twenty-week-old female mice were divided into three groups: medication with 17β-estradiol after ovariectomy (OVX + 17β-estradiol), ovariectomy (OVX), and sham (SHAM). After 4 weeks, the mice received two full-thickness wounds. Then, the OVX + 17β-estradiol group was administered 17β-estradiol at 0.01 g/day until healing. The ratio of wound area in the OVX + 17β-estradiol group was significantly decreased compared with that in the OVX group. The numbers of neutrophils and macrophages in the OVX + 17β-estradiol group were significantly smaller than those in the OVX group. In addition, the ratio of myofibroblasts in the OVX + 17β-estradiol group was significantly higher than that in the OVX group. These data suggested that exogenous continuous 17β-estradiol administration promotes cutaneous wound healing in 24-week OVX female mice by reducing wound area, shortening inflammatory response, and promoting wound contraction. However, it is unclear whether the effect of exogenous estrogen on wound healing outweighs the delay of wound healing due to advanced age.

scholarly journals MicroRNA-200b/c-3p regulate epithelial plasticity and inhibit cutaneous wound healing by modulating TGF-β-mediated RAC1 signaling

2020 ◽  
Vol 11 (10) ◽  
Author(s):  
Huiyi Tang ◽  
Xueer Wang ◽  
Min Zhang ◽  
Yuan Yan ◽  
Simin Huang ◽  
...  
Keyword(s):  
Wound Healing ◽  
Luciferase Reporter ◽  
Skin Wounds ◽  
Cutaneous Wound Healing ◽  
Mirna Regulation ◽  
Cutaneous Wound ◽  
Cutaneous Wounds ◽  
Keratinocyte Migration ◽  
Epithelial Plasticity ◽  
Tgf Β1

Abstract Cutaneous wound healing is pivotal for human skin to regain barrier function against pathogens. MicroRNAs (miRNAs) have been found to play regulatory roles in wound healing. However, the mechanism of miRNA regulation remains largely unknown. In this study, we focused on microRNA-200b/c-3p (miR-200b/c-3p) whose expression was abundant in intact epidermis, but dramatically decreased in skin wounds. In silico prediction identified RAC1 as a potential miR-200b/c-3p target. Luciferase reporter assay confirmed that miR-200b/c-p repressed RAC1 by direct targeting to its mRNA 3′UTR. Consistently, miR-200b/c-3p expression was discordantly related to RAC1 protein level during wound healing. Forced miR-200b/c-3p expression repressed RAC1 and inhibited keratinocyte migration as well as re-epithelialization in a mouse back skin full-thickness wound healing model. Mechanistically, miR-200b/c-3p modulated RAC1 to inhibit cell migration by repressing lamellipodia formation and intercellular adhesion dissolution in keratinocytes. Furthermore, we found that TGF-β1, which was highly expressed in skin wounds, contributed to the downregulation of miR-200b/c-3p in wound edge keratinocytes. Taken together, miR-200b/c-3p-mediated RAC1 repression inhibited keratinocyte migration to delay re-epithelialization. TGF-β1 induction attenuated miR-200b/c-3p regulation of RAC1 signaling in cutaneous wounds and the repression of miR-200b/c-3p accelerated keratinocyte migration to promote wound healing. Our data provide new insight into how miR-200b/c-3p affects keratinocyte migration and highlight the potential of miR-200b/c-3p targeting for accelerating wound healing.

scholarly journals Both obesity-prone and obesity-resistant rats present delayed cutaneous wound healing

2011 ◽  
Vol 106 (4) ◽  
pp. 603-611 ◽  
Author(s):  
Adriana Paulino do Nascimento ◽  
Andréa Monte-Alto-Costa
Keyword(s):  
Wound Healing ◽  
Saturated Fat ◽  
Inflammatory Cells ◽  
Male Rats ◽  
Control Group ◽  
Cutaneous Wound Healing ◽  
Cutaneous Wound ◽  
Diet Induced Obesity ◽  
Tnf Α ◽  
Obesogenic Diet

Diet-induced overweight rats exhibit delayed cutaneous healing; however, when receiving an obesogenic diet, some rats are susceptible to developing the overweight phenotype, whereas others are resistant. We investigated cutaneous healing in diet-induced obesity (DIO)-prone and diet-resistant (DR) rats. Male rats were fed with a standard (control) or a high-saturated fat (30 % fat, w/w) diet for 20 weeks. Then, the experimental group was subdivided into DIO (n 17) and DR (n 16) groups. An excision lesion was made, and the animals were killed 7 or 14 d later. The average body weight was 29 and 25 % higher in the DIO group compared with the C and DR groups. Retroperitoneal fat was higher in the DIO group than in the control and DR groups (518 and 92 %) and was higher in the DR group than in the control group (223 %). The DIO group presented glucose intolerance, and both the DIO and DR groups presented delayed wound contraction (50 %) and re-epithelialisation (20 %). Compared with the DR group, the DIO group displayed higher amounts of inflammatory cells as well as higher levels of lipid peroxidation (P < 0·05). Myofibroblastic differentiation and vessel remodelling were delayed in both the DIO and DR groups. Nitrite levels were lower in the DIO group (340 % less) than in the DR group. TNF-α expression was increased in the DIO group (130 %) compared with the DR group. Our results showed that DIO as well as DR rats present delays in cutaneous wound healing, even though the DR group does not have an overweight phenotype.

Sign in / Sign up

Export Citation Format

Share Document