Exenatide inhibits necrosis by enhancing angiogenesis and ameliorating ischemia/reperfusion injury in a random skin flap rat model
Exenatide inhibits necrosis by enhancing angiogenesis and ameliorating ischemia/reperfusion injury in a random skin flap rat model
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DOI：
10.1016/j.intimp.2020.107192
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发表时间：
2021-01-12
影响因子：
5.6
通讯作者：
Lin, Ding-Sheng
中科院分区：
文献类型：
--
作者：
He, Ji-Bing;Ma, Xin-Yi;Lin, Ding-Sheng
背景：随意皮瓣因其方便灵活，常用于整形修复。然而，皮瓣坏死是一种常见的并发症，可能导致灾难性的后果。艾塞那肽是一种胰高血糖素样肽1受体激动剂，可增强血管生成，改善缺血/再灌注损伤。我们的实验探讨了随机皮瓣的结果后，其use.Methods：我们建立了改良背McFarlane皮瓣54 Sprague-Dawley大鼠，并将大鼠分为三组（对照组，执行-I，和执行-II）。我们腹腔注射4或8 μ g/kg/天exenglutamine到大鼠的Exe-I和Exe-II组，分别。于术后第7天测定超氧化物歧化酶（SOD）和丙二醛（MDA）的含量。组织切片进行组织病理学和免疫组织化学分析，我们评估了血管内皮生长因子（VEGF），白细胞介素（IL）6，IL-1 β，核因子κ β（NF-κ B），Toll样受体4（TLR 4）和肿瘤坏死因子α（TNF-α）的表达。结果：Exenetine可明显增加皮瓣的平均成活面积，并呈剂量依赖性地提高微血管密度和血流强度。同时，SOD水平上调，MDA水平下调。Exenglutamine还增强了VEGF的表达，并减少了炎症细胞因子（IL-6，IL-1 β，NF-κ B，TLR 4和TNF-α）的表达，从而促进血管生成和抑制inflammation.Conclusions：Exenglutamine潜在地抑制我们的大鼠随机皮瓣模型中的坏死。
Background: Random skin flaps are often used for plastic repair because they are convenient and flexible. However, necrosis of flaps is a common complication that may lead to disastrous consequences. Exenatide, a glucagon-like peptide 1 receptor agonist, can enhance angiogenesis and ameliorate ischemia/reperfusion injury. Our experiments explored random skin flap outcomes after its use.Methods: We established modified dorsal McFarlane flaps on 54 Sprague-Dawley rats and divided the rats into three groups (control, Exe-I, and Exe-II). We intraperitoneally injected either 4 or 8 mu g/kg/day exenatide into the rats of the Exe-I and Exe-II groups, respectively. On the seventh day after the operation, we measured the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). Tissue sections were obtained for histopathological and immunohistochemical analyses, and we evaluated the expression of vascular endothelial growth factor (VEGF), interleukin (IL) 6,IL-1 beta, nuclear factor kappa beta (NF-kappa B), Toll-like receptor 4 (TLR4), and tumor necrosis factor alpha (TNF-alpha). We measured blood flow reconstruction and angiogenesis using laser Doppler blood flowmetry and lead oxide/gelatin angiography, respectively.Results: Exenatide increased the average survival area of the flap and improved microvascular density and blood flow intensity in a dose-dependent manner. Meanwhile, the SOD level was up-regulated and the MDA level down-regulated. Exenatide also enhanced the expression of VEGF and reduced the expression of inflammatory cytokines (IL-6, IL-1 beta, NF-kappa B, TLR4, and TNF-alpha), thereby promoting angiogenesis and inhibiting inflammation.Conclusions: Exenatide potentially inhibits necrosis in our rat random skin flap model.