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[1]鄭平,王東鵬.三甲胺-N-氧化物協(xié)同RAS誘導(dǎo)動(dòng)脈粥樣硬化發(fā)展機(jī)制研究[J].福建醫(yī)藥雜志,2023,45(01):96-102.
　ZHENG Ping,WANG Dongpeng.Study on the development mechanism of action of TMAO cooperating RAS system to induce atherosclerosis[J].FUJIAN MEDICAL JOURNAL,2023,45(01):96-102.
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三甲胺-N-氧化物協(xié)同RAS誘導(dǎo)動(dòng)脈粥樣硬化發(fā)展機(jī)制研究()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年01期
頁(yè)碼:
96-102
欄目:
基礎(chǔ)研究
出版日期:
2023-02-15

文章信息/Info

Title:
Study on the development mechanism of action of TMAO cooperating RAS system to induce atherosclerosis
文章編號(hào):
1002-2600(2023)01-0096-07
作者:
鄭平; 王東鵬
福建中醫(yī)藥大學(xué)附屬福州中醫(yī)院(福州 350004)
Author(s):
ZHENG Ping;  WANG Dongpeng
Fuzhou Hospital of Traditional Chinese Medicine Affiliated to Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350004, China
關(guān)鍵詞:
三甲胺-N-氧化物;  RAS系統(tǒng);  人臍靜脈內(nèi)皮細(xì)胞;  血管緊張素Ⅱ
Keywords:
Trimethylamine-N-oxide;  RAS system;  HUVECs;  AngiotensinⅡ
分類(lèi)號(hào):
R543.5
文獻(xiàn)標(biāo)志碼:
A
摘要:
目的 探究三甲胺-N-氧化物(TMAO)與腎素-血管緊張素系統(tǒng)(RAS)在人臍靜脈內(nèi)皮細(xì)胞(HUVECs)炎癥中的關(guān)系及作用機(jī)制。方法 采用分子克隆技術(shù),構(gòu)建血管緊張素Ⅱ(AngⅡ)過(guò)表達(dá)和敲減的HUVECs; TMAO干預(yù)上述HUVECs后,檢測(cè)細(xì)胞中炎癥因子及細(xì)胞增殖、遷移、血管形成能力,并分析細(xì)胞中RAS重要組分的表達(dá)水平。結(jié)果 成功構(gòu)建了AngⅡ過(guò)表達(dá)和敲減的HUVECs; AngⅡ過(guò)表達(dá)促進(jìn)TMAO調(diào)節(jié)HUVECs炎癥,抑制HUVECs增殖,抑制HUVECs遷移能力,抑制HUVECs血管形成,促進(jìn)細(xì)胞中RAS組分AGT、ACE、AngⅡ、ATR的表達(dá); 敲減AngⅡ抑制TMAO調(diào)節(jié)HUVECs炎癥,促進(jìn)HUVECs增殖,促進(jìn)HUVECs遷移能力,促進(jìn)HUVECs細(xì)胞的血管形成,抑制細(xì)胞中RAS組分AGT、ACE、AngⅡ、ATR的表達(dá)。結(jié)論 TMAO能夠協(xié)同RAS誘導(dǎo)HUVECs炎癥。
Abstract:
Objective To explore the relationship and mechanism of TMAO and RAS in HUVECs inflammation. Methods Molecular cloning technology was used to construct overexpression and knockdown HUVECs of AngⅡ. After TMAO interfering with HUVECs, the inflammatory factors in cells, the ability of cell proliferation, and migration and angiogenesis were detected, and the expression level of RAS important components in cells was analyzed. Results Overexpression and knockdown HUVECs of AngⅡwere successfully constructed. Overexpression of AngⅡpromoted TMAO to regulate HUVECs inflammation, inhibited HUVECs proliferation, inhibited HUVECs migration ability, inhibited HUVECs angiogenesis, promoted the expression of RAS components AGT, ACE, AngⅡ, and ATR in cells. Knockdown of AngⅡinhibited TMAO to regulate HUVECs inflammation,promoted HUVECs proliferation, promoted HUVECs migration ability, promoted HUVECs angiogenesis, and inhibited the expression of RAS components AGT, ACE, AngⅡ, and ATR in cells. Conclusion TMAO can cooperate with RAS to induce HUVECs inflammation.

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備注/Memo:
基金項(xiàng)目:福州市市級(jí)科技計(jì)劃項(xiàng)目(2019-SZ-29)
更新日期/Last Update: 2023-02-15