Pre- and/or Postsurgical Administration of Estradiol Benzoate Increases Skin Flap Viability in Female Rats

Vasilenko, Tomáš; Slezák, Martin; Novotný, Martin; Kováč, Ivan; Ďurkáč, Ján; Tomková, Iveta; Torma, N; Vrzgula, A; Lenhardt, L; Levkut, Mikukáš; Gál, Péter

doi:10.1007/s00266-013-0151-z

Cited by 6 publications

(5 citation statements)

References 26 publications

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“…In the present study, we showed for the first time, to our knowledge, that genistein is able to significantly increase skin flap viability in female rats. Similarly as seen in two previous estrogen papers [ 2 , 16 ], the maximal protection was maintained with a 3-day pretreatment and not when initiated at the day of flap surgery. Therefore, it may be speculated that functional and/or structural changes in skin and/or vasculature seemed to be a prerequisite for the protective effect of genistein.…”

Section: Discussionsupporting

confidence: 74%

Genistein Improves Skin Flap Viability in Rats: A Preliminary In Vivo and In Vitro Investigation

et al. 2018

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Selective estrogen receptor modulators (SERMs) have been developed to achieve beneficial effects of estrogens while minimizing their side effects. In this context, we decided to evaluate the protective effect of genistein, a natural SERM, on skin flap viability in rats and in a series of in vitro experiments on endothelial cells (migration, proliferation, antioxidant properties, and gene expression profiling following genistein treatment). Our results showed that administration of genistein increased skin flap viability, but importantly, the difference is only significant when treatment is started 3 days prior the flap surgery. Based on our in vitro experiments, it may be hypothesized that the underlying mechanism may rather by mediated by increasing SOD activity and Bcl-2 expression. The gene expression profiling further revealed 9 up-regulated genes (angiogenesis/inflammation promoting: CTGF, CXCL5, IL-6, ITGB3, MMP-14, and VEGF-A; angiogenesis inhibiting: COL18A1, TIMP-2, and TIMP-3). In conclusion, we observed a protective effect of genistein on skin flap viability which could be potentially applied in plastic surgery to women undergoing a reconstructive and/or plastic intervention. Nevertheless, further research is needed to explain the exact underlying mechanism and to find the optimal treatment protocol.

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Section: Discussionsupporting

confidence: 74%

Genistein Improves Skin Flap Viability in Rats: A Preliminary In Vivo and In Vitro Investigation

et al. 2018

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“…Similarly, we showed in our previous study that estrogen replacement therapy increases skin flap viability in rats [41] by increasing VEGF expression and NO synthesis [42]. Furthermore, increased tissue survival may be related to iNOS-dependent enhancement of VEGF levels and resulting angiogenic response [43].…”

Section: Resultsmentioning

confidence: 75%

Agrimonia eupatoria L. and Cynara cardunculus L. Water Infusions: Phenolic Profile and Comparison of Antioxidant Activities

et al. 2015

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Abstract:Reactive oxygen species (ROS) are highly considered in the ethiopathogenesis of different pathological conditions because they may cause significant damage to cells and tissues. In this paper, we focused on potential antioxidant properties of two medical plants such as the Agrimonia eupatoria L. and Cynara cardunculus L. Both plants have previously been studied for their pharmacological activities, especially as hepatoprotective and hypoglycemic activities. It has been suggested, that their effects are related to the antioxidant properties of polyphenols, which are dominant compounds of the plants' extracts. In the present study HPLC-MS analysis of water infusion was performed allowing the identification of several phenolic constituents. Furthermore, antioxidant effects of the two extracts were compared showing higher effects for agrimony extract compared to artichoke. Thus, agrimony was selected for the in vivo study using the skin flap viability model. In conclusion, our results provide evidence that the A. eupatoria extract may be a valuable source of polyphenols to be studied for the future development of supplements useful in the prevention of diseases linked to oxidative stress.

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“…Studies have indicated that estradiol may exert a protective effect against I/R injury in the brain, heart, and gastrointestinal tract . A number of reports have also indicated that estradiol can reduce flap I/R injury and improve flap survival . The mechanism of this protective effect may involve regulation of the neutrophil inflammatory cascade, mitochondrial respiratory function, intracellular‐free calcium level, control of cell apoptosis, and/or the transmission of estrogen receptor signaling …”

Section: Introductionmentioning

confidence: 99%

“…13,32 A number of reports have also indicated that estradiol can reduce flap I/R injury and improve flap survival. 29,35,38 The mechanism of this protective effect may involve regulation of the neutrophil inflammatory cascade, mitochondrial respiratory function, intracellular-free calcium level, control of cell apoptosis, and/or the transmission of estrogen receptor signaling. 2,39 The mechanism of I/R injury may involve microvascular dysfunction, accumulation of oxygen free radicals, increased neutrophil activation and adhesion, release of inflammatory mediators (tumor necrosis factors [TNFs]), and the induction of cellular apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Role of the p38 mitogen‐activated protein kinase signaling pathway in estrogen‐mediated protection following flap ischemia‐reperfusion injury

Hou

2016

Cell Biochemistry & Function

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Ischemia-reperfusion (I/R) injury often occurs during skin flap transplantation and results in tissue damage. Although estrogen treatment significantly alleviates this I/R injury-induced damage, the detailed molecular mechanism is not clear. In this study, a superficial epigastric artery flap I/R injury model was created in adult Wistar rats. Severe necrosis was observed in skin tissue after I/R injury. Histological examination of skin tissue revealed that I/R injury damages skin structure and results in neutrophil infiltration. Inflammation-related parameters, including neutrophil count, tumor necrosis factor-α, and interleukin-10 levels, were increased due to I/R injury. These pathological phenomena were reduced by estradiol treatment. Further investigation found that I/R injury triggers the p38 mitogen-activated protein kinase (p38-MAPK) pathway. The expression levels of p38-MAPK and phosphorylated p38-MAPK were increased after I/R injury. Estradiol increased the expression level of MAPK phosphatase-2, a putative phosphatase of p38, and reduced the levels of p38-MAPK and phosphorylated p38-MAPK. These results suggest that estradiol can improve skin flap survival, possibly by inhibiting neutrophil infiltration and the expression of p38-MAPK. This study provides an explanation for how estrogen alleviates I/R injury-induced damage that occurs during skin flap transplantation. In a rat pathological model, I/R injury leads to skin necrosis, skin structure damage, neutrophil infiltration, and inflammatory cytokine secretion, which are probably downstream effects of activation of the p38-MAPK pathway. On the other hand, estradiol treatment triggers the expression of MAPK phosphatase-2, a putative phosphatase of p38-MAPK, and reduced all examined pathological phenomena. Therefore, estrogen may reduce the deleterious effect of I/R injury on skin flap transplantation through modulating the p38-MAPK pathway.

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Pre- and/or Postsurgical Administration of Estradiol Benzoate Increases Skin Flap Viability in Female Rats

Cited by 6 publications

References 26 publications

Genistein Improves Skin Flap Viability in Rats: A Preliminary In Vivo and In Vitro Investigation

Genistein Improves Skin Flap Viability in Rats: A Preliminary In Vivo and In Vitro Investigation

Agrimonia eupatoria L. and Cynara cardunculus L. Water Infusions: Phenolic Profile and Comparison of Antioxidant Activities

Role of the p38 mitogen‐activated protein kinase signaling pathway in estrogen‐mediated protection following flap ischemia‐reperfusion injury

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