scholarly journals 20(S)-Protopanaxadiol enhances angiogenesis via HIF-1α-mediated VEGF secretion by activating p70S6 kinase and benefits wound healing in genetically diabetic mice

2017 ◽  
Vol 49 (10) ◽  
pp. e387-e387 ◽  
Author(s):  
Er-Yun Zhang ◽  
Bo Gao ◽  
Hai-Lian Shi ◽  
Ling-Fang Huang ◽  
Li Yang ◽  
...  
2010 ◽  
Vol 22 (2) ◽  
pp. 61-67 ◽  
Author(s):  
Daichi Chikazu ◽  
Tetsushi Taguchi ◽  
Hiroyuki Koyama ◽  
Hisako Hikiji ◽  
Hisako Fujihara ◽  
...  

Author(s):  
Mariarosaria Galeano ◽  
Francesca Polito ◽  
Alessandra Bitto ◽  
Natasha Irrera ◽  
Giuseppe M. Campo ◽  
...  

2013 ◽  
Vol 125 (12) ◽  
pp. 575-585 ◽  
Author(s):  
Alessandra Bitto ◽  
Natasha Irrera ◽  
Letteria Minutoli ◽  
Margherita Calò ◽  
Patrizia Lo Cascio ◽  
...  

Diabetic mice are characterized by a disrupted expression pattern of VEGF (vascular endothelial growth factor), and impaired vasculogenesis during healing. Experimental evidence suggests that RLX (relaxin) can improve several parameters associated with wound healing. Therefore we investigated the effects of porcine-derived RLX in diabetes-related wound-healing defects in genetically diabetic mice. An incisional wound model was produced on the back of female diabetic C57BL/KsJ-m+/+Leptdb (db+/db+) mice and their normal littermates (db+/+m). Animals were treated daily with porcine RLX (25 μg/mouse per day, subcutaneously) or its vehicle. Mice were killed on 3, 6 and 12 days after skin injury for measurements of VEGF mRNA and protein synthesis, SDF-1α (stromal cell-derived factor-1α) mRNA and eNOS (endothelial NO synthase) expression. Furthermore, we evaluated wound-breaking strength, histological changes, angiogenesis and vasculogenesis at day 12. Diabetic animals showed a reduced expression of VEGF, eNOS and SDF-1α compared with non-diabetic animals. At day 6, RLX administration resulted in an increase in VEGF mRNA expression and protein wound content, in eNOS expression and in SDF-1α mRNA. Furthermore, the histological evaluation indicated that RLX improved the impaired wound healing, enhanced the staining of MMP-11 (matrix metalloproteinase-11) and increased wound-breaking strength at day 12 in diabetic mice. Immunohistochemistry showed that RLX in diabetic animals augmented new vessel formation by stimulating both angiogenesis and vasculogenesis. RLX significantly reduced the time to complete skin normalization and this effect was abrogated by a concomitant treatment with antibodies against VEGF and CXCR4 (CXC chemokine receptor 4), the SDF-1α receptor. These data strongly suggest that RLX may have a potential application in diabetes-related wound disorders.


Surgery ◽  
2011 ◽  
Vol 149 (2) ◽  
pp. 253-261 ◽  
Author(s):  
Domenica Altavilla ◽  
Francesco Squadrito ◽  
Francesca Polito ◽  
Natasha Irrera ◽  
Margherita Calò ◽  
...  

Diabetes ◽  
2003 ◽  
Vol 52 (11) ◽  
pp. 2805-2813 ◽  
Author(s):  
M. Peppa ◽  
H. Brem ◽  
P. Ehrlich ◽  
J.-G. Zhang ◽  
W. Cai ◽  
...  

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Ilya A. Demyanenko ◽  
Vlada V. Zakharova ◽  
Olga P. Ilyinskaya ◽  
Tamara V. Vasilieva ◽  
Artem V. Fedorov ◽  
...  

Oxidative stress is widely recognized as an important factor in the delayed wound healing in diabetes. However, the role of mitochondrial reactive oxygen species in this process is unknown. It was assumed that mitochondrial reactive oxygen species are involved in many wound-healing processes in both diabetic humans and animals. We have applied the mitochondria-targeted antioxidant 10-(6′-plastoquinonyl)decyltriphenylphosphonium (SkQ1) to explore the role of mitochondrial reactive oxygen species in the wound healing of genetically diabetic mice. Healing of full-thickness excisional dermal wounds in diabetic C57BL/KsJ-db−/db− mice was significantly enhanced after long-term (12 weeks) administration of SkQ1. SkQ1 accelerated wound closure and stimulated epithelization, granulation tissue formation, and vascularization. On the 7th day after wounding, SkQ1 treatment increased the number of α-smooth muscle actin-positive cells (myofibroblasts), reduced the number of neutrophils, and increased macrophage infiltration. SkQ1 lowered lipid peroxidation level but did not change the level of the circulatory IL-6 and TNF. SkQ1 pretreatment also stimulated cell migration in a scratch-wound assay in vitro under hyperglycemic condition. Thus, a mitochondria-targeted antioxidant normalized both inflammatory and regenerative phases of wound healing in diabetic mice. Our results pointed to nearly all the major steps of wound healing as the target of excessive mitochondrial reactive oxygen species production in type II diabetes.


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