rhaFGF通过抑制慢性炎症促进急性糖尿病伤口愈合。

IF 3.9 2区 综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES
Ting Pang, Yuankai Shao, Li Zhou, Zhibin Wang, Ping Xi, Yuan Zhang, Lihui Xie, Zhe Deng
{"title":"rhaFGF通过抑制慢性炎症促进急性糖尿病伤口愈合。","authors":"Ting Pang, Yuankai Shao, Li Zhou, Zhibin Wang, Ping Xi, Yuan Zhang, Lihui Xie, Zhe Deng","doi":"10.1038/s41598-025-03086-5","DOIUrl":null,"url":null,"abstract":"<p><p>To investigate the effect of recombinant human aFGF (rhaFGF) on acute wounds in a diabetic mouse model focusing on the transition from acute inflammation to chronic inflammation. Diabetes mellitus (DM) mouse models were induced through intraperitoneal injection of streptozotocin and acute diabetic wounds were created on their hind paws. The mice were divided into four groups: Con, Con + rhaFGF, DM, and DM + rhaFGF. rhaFGF (0.08 µg/cm²) or PBS was daily administered on wound surface for 14 days. The levels of IL-6 and TNF-α in serum and tissues were measured using ELISA, and NLRP3 inflammasome components (NLRP3, ASC and caspase-1) and pro-inflammatory cytokines (IL-1β, IL-18) in tissue were detected by Western blot analysis. CCK8 assay and cell migration were used to assess the proliferation and migration ability of HUVEC, HFF, and HaCaT cells, respectively. Wound healing rates in the DM group decreased significantly, which was effectively alleviated by rhaFGF treatment for 7 days and longer durations. Notably, at day 7 after wound creation, the levels of IL-6 and TNF-α as well as the expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the DM group were significantly increased, and rhaFGF treatment substantially suppressed these changes. Moreover, when HUVEC, HFF, and HaCaT cells were exposed to high glucose and LPS condition, the proliferation and migration of these cells were significantly inhibited, and rhaFGF treatment effectively reversed this inhibition. rhaFGF could promote the healing of acute DM wounds by preventing chronicity transition of acute inflammation via reducing the release of pro-inflammatory cytokines and inhibiting the activation of NLRP3 in DM wounds.</p>","PeriodicalId":21811,"journal":{"name":"Scientific Reports","volume":"15 1","pages":"19085"},"PeriodicalIF":3.9000,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125378/pdf/","citationCount":"0","resultStr":"{\"title\":\"rhaFGF promotes acute diabetic wound healing by suppressing chronicity of inflammation.\",\"authors\":\"Ting Pang, Yuankai Shao, Li Zhou, Zhibin Wang, Ping Xi, Yuan Zhang, Lihui Xie, Zhe Deng\",\"doi\":\"10.1038/s41598-025-03086-5\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>To investigate the effect of recombinant human aFGF (rhaFGF) on acute wounds in a diabetic mouse model focusing on the transition from acute inflammation to chronic inflammation. Diabetes mellitus (DM) mouse models were induced through intraperitoneal injection of streptozotocin and acute diabetic wounds were created on their hind paws. The mice were divided into four groups: Con, Con + rhaFGF, DM, and DM + rhaFGF. rhaFGF (0.08 µg/cm²) or PBS was daily administered on wound surface for 14 days. The levels of IL-6 and TNF-α in serum and tissues were measured using ELISA, and NLRP3 inflammasome components (NLRP3, ASC and caspase-1) and pro-inflammatory cytokines (IL-1β, IL-18) in tissue were detected by Western blot analysis. CCK8 assay and cell migration were used to assess the proliferation and migration ability of HUVEC, HFF, and HaCaT cells, respectively. Wound healing rates in the DM group decreased significantly, which was effectively alleviated by rhaFGF treatment for 7 days and longer durations. Notably, at day 7 after wound creation, the levels of IL-6 and TNF-α as well as the expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the DM group were significantly increased, and rhaFGF treatment substantially suppressed these changes. Moreover, when HUVEC, HFF, and HaCaT cells were exposed to high glucose and LPS condition, the proliferation and migration of these cells were significantly inhibited, and rhaFGF treatment effectively reversed this inhibition. rhaFGF could promote the healing of acute DM wounds by preventing chronicity transition of acute inflammation via reducing the release of pro-inflammatory cytokines and inhibiting the activation of NLRP3 in DM wounds.</p>\",\"PeriodicalId\":21811,\"journal\":{\"name\":\"Scientific Reports\",\"volume\":\"15 1\",\"pages\":\"19085\"},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2025-05-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12125378/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Scientific Reports\",\"FirstCategoryId\":\"103\",\"ListUrlMain\":\"https://doi.org/10.1038/s41598-025-03086-5\",\"RegionNum\":2,\"RegionCategory\":\"综合性期刊\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"MULTIDISCIPLINARY SCIENCES\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Scientific Reports","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1038/s41598-025-03086-5","RegionNum":2,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0

摘要

目的探讨重组人aFGF (rhaFGF)对糖尿病小鼠急性创面的影响,重点研究急性炎症向慢性炎症的转变。通过腹腔注射链脲佐菌素诱导糖尿病(DM)小鼠模型,并在其后爪上制造急性糖尿病创面。将小鼠分为Con、Con + rhaFGF、DM、DM + rhaFGF四组。每天在创面施用rhaFGF(0.08µg/cm²)或PBS,连续14天。ELISA法检测血清和组织中IL-6、TNF-α水平,Western blot法检测组织中NLRP3炎性小体成分(NLRP3、ASC、caspase-1)和促炎因子(IL-1β、IL-18)水平。采用CCK8法和细胞迁移法分别评估HUVEC、HFF和HaCaT细胞的增殖和迁移能力。DM组创面愈合率明显下降,rhaFGF治疗7天及以上可有效缓解。值得注意的是,在创面后第7天,DM组IL-6和TNF-α水平以及NLRP3、ASC、caspase-1、IL-1β和IL-18的表达均显著升高,而rhaFGF处理可显著抑制这些变化。此外,当HUVEC、HFF和HaCaT细胞暴露于高糖和LPS条件下时,这些细胞的增殖和迁移受到明显抑制,而rhaFGF处理有效地逆转了这种抑制。rhaFGF可能通过减少促炎细胞因子的释放和抑制NLRP3的激活,阻止急性炎症的慢性转变,从而促进急性DM伤口的愈合。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
rhaFGF promotes acute diabetic wound healing by suppressing chronicity of inflammation.

To investigate the effect of recombinant human aFGF (rhaFGF) on acute wounds in a diabetic mouse model focusing on the transition from acute inflammation to chronic inflammation. Diabetes mellitus (DM) mouse models were induced through intraperitoneal injection of streptozotocin and acute diabetic wounds were created on their hind paws. The mice were divided into four groups: Con, Con + rhaFGF, DM, and DM + rhaFGF. rhaFGF (0.08 µg/cm²) or PBS was daily administered on wound surface for 14 days. The levels of IL-6 and TNF-α in serum and tissues were measured using ELISA, and NLRP3 inflammasome components (NLRP3, ASC and caspase-1) and pro-inflammatory cytokines (IL-1β, IL-18) in tissue were detected by Western blot analysis. CCK8 assay and cell migration were used to assess the proliferation and migration ability of HUVEC, HFF, and HaCaT cells, respectively. Wound healing rates in the DM group decreased significantly, which was effectively alleviated by rhaFGF treatment for 7 days and longer durations. Notably, at day 7 after wound creation, the levels of IL-6 and TNF-α as well as the expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the DM group were significantly increased, and rhaFGF treatment substantially suppressed these changes. Moreover, when HUVEC, HFF, and HaCaT cells were exposed to high glucose and LPS condition, the proliferation and migration of these cells were significantly inhibited, and rhaFGF treatment effectively reversed this inhibition. rhaFGF could promote the healing of acute DM wounds by preventing chronicity transition of acute inflammation via reducing the release of pro-inflammatory cytokines and inhibiting the activation of NLRP3 in DM wounds.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Scientific Reports
Scientific Reports Natural Science Disciplines-
CiteScore
7.50
自引率
4.30%
发文量
19567
审稿时长
3.9 months
期刊介绍: We publish original research from all areas of the natural sciences, psychology, medicine and engineering. You can learn more about what we publish by browsing our specific scientific subject areas below or explore Scientific Reports by browsing all articles and collections. Scientific Reports has a 2-year impact factor: 4.380 (2021), and is the 6th most-cited journal in the world, with more than 540,000 citations in 2020 (Clarivate Analytics, 2021). •Engineering Engineering covers all aspects of engineering, technology, and applied science. It plays a crucial role in the development of technologies to address some of the world''s biggest challenges, helping to save lives and improve the way we live. •Physical sciences Physical sciences are those academic disciplines that aim to uncover the underlying laws of nature — often written in the language of mathematics. It is a collective term for areas of study including astronomy, chemistry, materials science and physics. •Earth and environmental sciences Earth and environmental sciences cover all aspects of Earth and planetary science and broadly encompass solid Earth processes, surface and atmospheric dynamics, Earth system history, climate and climate change, marine and freshwater systems, and ecology. It also considers the interactions between humans and these systems. •Biological sciences Biological sciences encompass all the divisions of natural sciences examining various aspects of vital processes. The concept includes anatomy, physiology, cell biology, biochemistry and biophysics, and covers all organisms from microorganisms, animals to plants. •Health sciences The health sciences study health, disease and healthcare. This field of study aims to develop knowledge, interventions and technology for use in healthcare to improve the treatment of patients.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信