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端粒酶基16肽疫苗(GV1001)对缺血再灌注损伤大鼠模型下腹壁岛状皮瓣存活能力的保护作用。

Protective effect of telomerase-based 16-mer peptide vaccine (GV1001) on inferior epigastric island skin flap survivability in ischaemia-reperfusion injury rat model.

作者信息

Lee Yung Ki, Nata'atmaja Beta Subakti, Kim Byung Hwi, Pak Chang Sik, Heo Chan Yeong

机构信息

a Department of Plastic & Reconstructive Surgery, College of Medicine , Kyung Hee University , Seoul , Korea.

b Department of Plastic and Reconstructive Surgery , Dr. Soetomo General Hospital ? Airlangga University School of Medicine , Surabaya , Indonesia.

出版信息

J Plast Surg Hand Surg. 2017 Jun;51(3):210-216. doi: 10.1080/2000656X.2016.1235046. Epub 2016 Sep 27.

DOI:10.1080/2000656X.2016.1235046
PMID:27670432
Abstract

BACKGROUND

Ischaemia-reperfusion injury (IRI) results in oxidative damage and a profound inflammatory reaction, leading to cell death. GV 1001 is a telomerase-based 16-mer peptide vaccine developed against cancer. However, it has also been reported to possess antioxidant and anti-inflammatory properties. The aim of this study was to determine if GV 1001 can reduce the negative effects caused by IRI in a rat skin flap model owing to its anti-oxidant and anti-inflammatory properties.

MATERIALS AND METHODS

In order to evaluate the effect of GV 1001, 5 × 5 cm inferior epigastric artery based island skin flaps were dissected in 39 8-week-old Sprague-Dawley rats weighing 220-270 g. The rats were divided into three groups: (I) non-ischaemic group; (II) IRI with saline; and (III) IRI with 10 mg GV 1001 treatment. Drugs were administered intra-muscularly directly before and after ischaemia. Flap survival area, neutrophil infiltration, cytokine levels (interleukin [IL]-1, IL-6, and tumour necrosis factor-α), malondialdehyde (MDA) level, and superoxide dismutase (SOD) activity were measured. Flap survivability was analysed at 7 days after surgery.

RESULTS

Flap survival area was significantly larger in group III than in group II. Cytokine release level was also significantly lower in group III. Neutrophil infiltration grade, MDA level, and SOD activity slightly decreased in Group III; however, the changes were not statistically significant.

CONCLUSION

These results imply that GV 1001 exerts a protective effect against IRI through antioxidant effects, reducing reactive oxygen species, and suppressing the inflammatory cascade.

摘要

背景

缺血再灌注损伤(IRI)会导致氧化损伤和严重的炎症反应,进而引发细胞死亡。GV 1001是一种针对癌症开发的基于端粒酶的16肽疫苗。然而,也有报道称它具有抗氧化和抗炎特性。本研究的目的是确定GV 1001是否因其抗氧化和抗炎特性而能减轻大鼠皮瓣模型中IRI所造成的负面影响。

材料与方法

为评估GV 1001的作用,在39只体重220 - 270克的8周龄Sprague-Dawley大鼠身上解剖以腹壁下动脉为蒂的5×5厘米岛状皮瓣。大鼠被分为三组:(I)非缺血组;(II)缺血再灌注并用生理盐水处理组;(III)缺血再灌注并用10毫克GV 1001处理组。在缺血前后直接肌肉注射药物。测量皮瓣存活面积、中性粒细胞浸润、细胞因子水平(白细胞介素[IL]-1、IL-6和肿瘤坏死因子-α)、丙二醛(MDA)水平以及超氧化物歧化酶(SOD)活性,并在术后7天分析皮瓣存活率。

结果

III组皮瓣存活面积显著大于II组,III组细胞因子释放水平也显著更低。III组中性粒细胞浸润分级、MDA水平及SOD活性略有下降,但变化无统计学意义。

结论

这些结果表明,GV 1001通过抗氧化作用、减少活性氧并抑制炎症级联反应对IRI发挥保护作用。

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