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[1]張燕琴,董菲艷,劉學(xué)鋒.泛素特異性肽酶20通過調(diào)節(jié)TGF-β1/SMAD 3級聯(lián)反應(yīng)緩解膿毒癥性急性肺損傷中的氧化應(yīng)激和炎癥[J].福建醫(yī)藥雜志,2024,46(08):75-78,87.[doi:10.20148/j.fmj.2024.08.022]
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泛素特異性肽酶20通過調(diào)節(jié)TGF-β1/SMAD 3級聯(lián)反應(yīng)緩解膿毒癥性急性肺損傷中的氧化應(yīng)激和炎癥()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
46
期數(shù):
2024年08期
頁碼:
75-78,87
欄目:
基礎(chǔ)研究
出版日期:
2024-12-20

文章信息/Info

文章編號:
1002-2600(2024)08-0075-04
作者:
張燕琴董菲艷劉學(xué)鋒
寧德師范學(xué)院附屬寧德市醫(yī)院,寧德 352000
關(guān)鍵詞:
膿毒性急性肺損傷 USP20 炎癥 氧化應(yīng)激
分類號:
R563.1
DOI:
10.20148/j.fmj.2024.08.022
文獻標(biāo)志碼:
A
摘要:
目的 本研究旨在探討泛素特異性肽酶20(USP20)在膿毒癥性急性肺損傷(ALI)中的作用及具體機制。方法 分別用BEAS-2B細胞和C57BL/6小鼠建立體內(nèi)和體外脂多糖(LPS)處理的ALI模型。RT-qPCR檢測USP20的表達情況,在體外實驗?zāi)P椭修D(zhuǎn)染USP20腺病毒后,通過ELISA、CCK8和蛋白質(zhì)印跡等方法觀察其對ALI細胞模型的炎癥、氧化應(yīng)激、生存力等的影響。在USP20過表達治療后的體內(nèi)模型中,進一步觀察病理變化情況。結(jié)果 在ALI小鼠模型、LPS處理的BEAS-2B細胞中證實低表達USP20; 上調(diào)USP20可阻止炎癥和氧化應(yīng)激,同時增強了LPS處理的BEAS-2B細胞的生存能力; 上調(diào)的USP20通過抑制TGF-β1/SMAD3級聯(lián)激活減輕ALI小鼠的肺損傷。結(jié)論 USP20通過調(diào)節(jié)TGF-β1/SMAD3級聯(lián)反應(yīng)緩解膿毒癥性ALI的氧化應(yīng)激和炎癥。

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更新日期/Last Update: 2024-12-20