Exenatide inhibits necrosis by enhancing angiogenesis and ameliorating ischemia/reperfusion injury in a random skin flap rat model

He, Jibing; Ma, Xinyi; Li, Wenjie; Liu, Yingying; Lin, Dingsheng

doi:10.1016/j.intimp.2020.107192

Cited by 13 publications

(10 citation statements)

References 29 publications

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“…Therefore, the most important factor in protecting flap survival is to promote angiogenesis (Zhu X. et al, 2021;Lou et al, 2021). However, the adverse effects of I/R injury and nutrient deficiency during angiogenesis should not be ignored (Basu et al, 2014;He et al, 2021). Our findings showed that NT was the core factor for the survival of random flaps.…”

Section: Discussionmentioning

confidence: 74%

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Huang

Luo

Zhang

et al. 2021

Front. Bioeng. Biotechnol.

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Random flaps are widely used in tissue reconstruction, attributed to the lack of vascular axial limitation. Nevertheless, the distal end of the flap is prone to necrosis due to the lack of blood supply. Notoginseng triterpenes (NTs) are the active components extracted from Panax notoginseng, reducing oxygen consumption and improving the body’s tolerance to hypoxia. However, their role in random flap survival has not been elucidated. In this study, we used a mouse random skin flap model to verify that NT can promote cell proliferation and migration and that increasing blood perfusion can effectively improve the survival area of a skin flap. Our study also showed that the autophagy of random flaps after NT treatment was activated through the Beclin-1/VPS34/LC3 signaling pathway, and the therapeutic effect of NT significantly decreased after VPS34 IN inhibited autophagy. In conclusion, we have demonstrated that NT can significantly improve the survival rate of random flaps through the Beclin-1/VPS34/LC3 signaling pathway, suggesting that it might be a promising clinical treatment option.

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Section: Discussionmentioning

confidence: 74%

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Huang

Luo

Zhang

et al. 2021

Front. Bioeng. Biotechnol.

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“…Oxidative stress, inflammation, apoptosis, and lack of new blood vessels caused by a hypoxia state during ischemia and reperfusion in the transplantation process are the main threats to free flaps [ 31 , 32 ]. Pharmaceutical targeting all these processes can protect skin flaps from partial necrosis.…”

Section: Discussionmentioning

confidence: 99%

Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviate Ischemia-Reperfusion Injury and Promote Survival of Skin Flaps in Rats

Niu

Yang

et al. 2022

Life

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Free tissue flap transplantation is a classic and important method for the clinical repair of tissue defects. However, ischemia-reperfusion (IR) injury can affect the success rate of skin flap transplantation. We used a free abdomen flap rat model to explore the protective effects of exosomes derived from bone marrow mesenchymal stem cells (BMSCs-exosomes) against the IR injury of the skin flap. Exosomes were injected through the tail vein and the flaps were observed and obtained on day 7. We observed that BMSCs-exosomes significantly reduced the necrotic lesions of the skin flap. Furthermore, BMSCs-exosomes relieved oxidative stress and reduced the levels of inflammatory factors. Apoptosis was evaluated via the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and Western blot analysis of Bax, Bcl-2. Simultaneously, BMSCs-exosomes promoted the formation of new blood vessels in the IR flap, as confirmed by the increased expression level of VEGFA and the fluorescence co-staining of CD31 and PCNA. Additionally, BMSCs-exosomes considerably increased proliferation and migration of human umbilical vein endothelial cells and promoted angiogenesis in vitro. BMSCs-exosomes could be a promising cell-free therapeutic candidate to reduce IR injury and promote the survival of skin flaps.

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“…Exendin-4 was found to directly regulate endothelial cell migration, formation of tubes and ejection, In the human umbilical vein, this can promote the increase in cell numbers, and the increase in the creation of new blood vessels. Exendin-4 has been reported to promote angiogenesis and inhibit inflammation by increased VEGF (vascular endothelial growth factor) expression and decreased inflammatory cytokines (NF-κB, IL-6, TLR4, IL-1 and TNF-α) expression [5].…”

Section: Angiogenesismentioning

confidence: 99%

“…Due to these properties, it has been approved for clinical treatment of type II diabetes [4]; In addition to its benefits in treating asthma, tumors, and other chronic inflammatory diseases, it has also been found to have preventative effects against cardiovascular and neurological complications. Studies have shown that this medication has other beneficial effects too, such as promoting tissue regeneration, stimulating the migration of endothelial cells, inhibiting cell apoptosis, significantly increased vascular density and promotion of fibroblast migration and differentiation [5].…”

Section: Introductionmentioning

confidence: 99%

Mechanism of exendin-4 promoting bone regeneration

Guo

2024

Third International Conference on Biological Engineering and Medical Science (ICBioMed2023)

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Exendin-4 is an analogue of glucagon-like peptide-1 (GLP-1) and has a good efficacy in the treatment of type Ⅱ diabetes. Recently, some researchers have found that Exendin-4 can promote cell osteogenesis and angiogenesis, but the specific mechanism of its promotion of bone regeneration is not yet clear. This review focuses on the specific mechanisms by which Exendin-4 promotes osteogenesis in bone cells and stem cells, as well as its ability to induce endothelial cell migration, budding, and neovascularization, and promote angiogenesis. In addition, this article discusses some in vivo experiments using Exendin-4 alone or in combination with other materials. However, since its specific mechanism is not yet clear, and there is no clinical data to support it, a comprehensive understanding of the mechanism by which Exendin-4 promotes bone regeneration is of significant value for treatment of bone tissue damage in diabetic patients. This review also provides a certain direction and basis for the subsequent practical application of Exendin-4.

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Exenatide inhibits necrosis by enhancing angiogenesis and ameliorating ischemia/reperfusion injury in a random skin flap rat model

Cited by 13 publications

References 29 publications

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

Exosomes Derived from Bone Marrow Mesenchymal Stem Cells Alleviate Ischemia-Reperfusion Injury and Promote Survival of Skin Flaps in Rats

Mechanism of exendin-4 promoting bone regeneration

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