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西他列汀诱导的自噬对多区域穿支皮瓣存活的有害影响。

Detrimental Effect of Sitagliptin Induced Autophagy on Multiterritory Perforator Flap Survival.

作者信息

Chen Zhengtai, Zhang Chenxi, Ma Haiwei, Huang Zihuai, Li Jiafeng, Lou Junshen, Li Baolong, Tu Qi, Gao Weiyang

机构信息

Department of Orthopaedics, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, China.

Department of Orthopaedics, Zhejiang Provincial Key Laboratory of Orthpaedics, Wenzhou, China.

出版信息

Front Pharmacol. 2020 Jun 26;11:951. doi: 10.3389/fphar.2020.00951. eCollection 2020.

DOI:10.3389/fphar.2020.00951
PMID:32670067
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7332881/
Abstract

Multiterritory perforator flap survival is commonly applied in surgical tissue reconstructions and covering of large skin defects. However, multiple risk factors such as ischemia, reperfusion injury, and apoptosis after reconstructive surgeries cause necrosis in distal parts with outcomes ranging from poor aesthetic appearance to reconstructive failure. A few studies have reported that sitagliptin (Sit) promotes angiogenesis and inhibits apoptosis. However, little is known about Sit-induced autophagy especially on the flap model. Therefore, our study investigated the effect of Sit and its induced autophagy on the perforator flap survival. Ninety male Sprague-Dawley rats were randomly separated into control, Sit, and Sit+3-methyladenine group. Results revealed that Sit significantly promoted flap survival by enhancing angiogenesis, reducing oxidative stress, and attenuating apoptosis. In addition, flap survival was further improved after co-administration with 3-methyladenine to inhibit autophagy. Overall, our results established that Sit has positive effects in promoting survival of multiterritory perforator flap. Sit-induced autophagy was detrimental for flap survival and its inhibition may further improve flap survival.

摘要

多区域穿支皮瓣存活常用于外科组织重建和大面积皮肤缺损的覆盖。然而，诸如缺血、再灌注损伤以及重建手术后的细胞凋亡等多种风险因素会导致远端部位坏死，其结果从美观不佳到重建失败不等。一些研究报道，西他列汀（Sit）可促进血管生成并抑制细胞凋亡。然而，关于Sit诱导的自噬，尤其是在皮瓣模型上的情况，人们了解甚少。因此，我们的研究探讨了Sit及其诱导的自噬对穿支皮瓣存活的影响。将90只雄性Sprague-Dawley大鼠随机分为对照组、Sit组和Sit+3-甲基腺嘌呤组。结果显示，Sit通过增强血管生成、减轻氧化应激和减弱细胞凋亡，显著促进了皮瓣存活。此外，与3-甲基腺嘌呤联合给药以抑制自噬后，皮瓣存活进一步改善。总体而言，我们的结果表明，Sit在促进多区域穿支皮瓣存活方面具有积极作用。Sit诱导的自噬对皮瓣存活有害，抑制自噬可能会进一步提高皮瓣存活率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/8a35ad411793/fphar-11-00951-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/5ab9134b0731/fphar-11-00951-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/d3f77fca79e5/fphar-11-00951-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/a3142954a4a1/fphar-11-00951-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/1a86934546db/fphar-11-00951-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/5b745d8e3a81/fphar-11-00951-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/8a35ad411793/fphar-11-00951-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/5ab9134b0731/fphar-11-00951-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/af82fef7db2c/fphar-11-00951-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/d3f77fca79e5/fphar-11-00951-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/a3142954a4a1/fphar-11-00951-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/1a86934546db/fphar-11-00951-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/5b745d8e3a81/fphar-11-00951-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7493/7332881/8a35ad411793/fphar-11-00951-g007.jpg

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