陈舒婷,刘远凤,张瑛,曹运长,封少龙.大蒜素改善PM2.5暴露诱导的HUVEC自噬损伤.[J].中南医学科学杂志.,2024,(2):163-166.
大蒜素改善PM2.5暴露诱导的HUVEC自噬损伤
Allicin improves HUVEC autophagic damage induced by PM2.5 exposure
投稿时间:2023-04-20  修订日期:2024-01-21
DOI:10.15972/j.cnki.43-1509/r.2024.02.002
中文关键词:  大蒜素  PM2.5  人脐静脉内皮细胞  自噬 [
英文关键词:allicin  PM2.5  human umbilical vein endothelial cells  autophagy
基金项目:国家自然科学基金(41877390);有机地球化学国家重点实验室开放课题(SKLOG202213) 作者简介:陈舒婷,硕士研究生,住院医师,研究方向为大气细颗粒物对心血管系统健康的影响与分子机制,E-mail为2210763025@qq.com。通信作者封少龙,博士,教授,硕士研究生导师,研究方向为环境毒害污染物对人体健康的影响与分子机制,E-mail为slfeng@glmc.edu.cn。
作者单位E-mail
陈舒婷 南华大学衡阳医学院公共卫生学院,湖南衡阳 421001
桂林医学院公共卫生学院预防医学研究所,广西桂林541199 
e-mail为2210763025@qq.com,e-mail为slfeng@glmc.edu.cn 
刘远凤 南华大学衡阳医学院公共卫生学院,湖南衡阳 421001  
张瑛 桂林医学院公共卫生学院预防医学研究所,广西桂林541199  
曹运长 桂林医学院公共卫生学院预防医学研究所,广西桂林541199  
封少龙 南华大学衡阳医学院公共卫生学院,湖南衡阳 421001
桂林医学院公共卫生学院预防医学研究所,广西桂林541199
中国科学院广州地球化学研究所 有机地球化学国家重点实验室,广东广州 510640 
e-mail为2210763025@qq.com,e-mail为slfeng@glmc.edu.cn 
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中文摘要:
      目的研究大蒜素改善细颗粒物(PM2.5)暴露损伤人脐静脉内皮细胞(HUVEC)自噬的机制。 方法将HUVEC分为对照组、PM2.5组(5 mg/L)、大蒜素组(10 mg/L)和联合组(10 mg/L大蒜素与5 mg/L PM2.5)。采用透射电镜观察各组自噬小体数;采用细胞免疫荧光、免疫印迹方法检测LC3、p62针点数和p62、p38、Beclin 1、LC3BⅡ/Ⅰ蛋白表达及p38蛋白的磷酸化水平。 结果与对照组比较,PM2.5组细胞活力明显降低,自噬小体数增加,Beclin 1、LC3BⅡ/Ⅰ和p62蛋白表达升高(P<0.05)。与PM2.5组比较,联合组细胞活力升高,自噬小体数减少,Beclin 1、LC3BⅡ/Ⅰ和p62蛋白表达及p38蛋白磷酸化水平降低(P<0.05)。 结论大蒜素改善PM2.5对HUVEC的损伤,可能与抑制p38蛋白磷酸化,促进PM2.5抑制的自噬流有关。
英文摘要:
      AimTo investigate the mechanism of allicin on PM2.5-induced autophagy in human umbilical vein endothelial cells (HUVEC). MethodsHUVEC were divided into control group, PM2.5 group (5 mg/L), allicin group (10 mg/L) and allicin combined group (10 mg/L allicin and 5 mg/L PM2.5). The number of autophagosomes in each group was observed by transmission electron microscopy.The needle count of LC3, p62 and the protein expressions of p62, p38, Beclin 1, LC3B Ⅱ/Ⅰ and the phosphorylation level of p38 were detected by cell immunofluorescence and Western blotting. ResultsCompared with the control group, the cell viability of PM2.5 group was significantly decreased, whereas the number of autophagosomes was increased and the protein expressions of Beclin 1, LC3BⅡ/Ⅰ and p62 were increased (P<0.05). Compared with the PM2.5 group, the cell viability of allicin combined group was increased, the number of autophagosomes was decreased, and the protein levels of Beclin 1, LC3BⅡ/Ⅰ and p62, as well as the phosphorylation level of p38 were decreased (P<0.05). ConclusionAllicin improves PM2.5-induced HUVEC injury, which may be related with the inhibition of phosphorylation of p38 protein and promotion of autophagy flow inhibited by PM2.5.
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