枸杞多糖通过抑制氧化应激、内质网应激和自噬来保护pm2.5诱导的HaCaT细胞凋亡。

IF 5.2 2区 生物学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY
Sen Zhu, Xuan Li, Bingrong Dang, Fen Wu, Chunming Wang, Changjun Lin
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引用次数: 25

摘要

目的:枸杞多糖(Lycium barbarum多糖,LBP)是从枸杞中提取的天然多糖,具有抗炎、抗细胞凋亡、抗衰老等作用,对多种疾病有预防和治疗作用。在这项研究中,我们研究了枸杞多糖对PM2.5引起的皮肤损伤的治疗作用。方法:采用MTT法和LDH法测定细胞活力。Annexin V-FITC/PI染色分析细胞凋亡。通过细胞内ROS水平、MDA含量和SOD活性评估氧化应激/损伤。Western blot检测细胞内蛋白表达。采用JC-1探针,采用线粒体膜电位检测线粒体损伤。将LC3-GFP腺病毒转染HaCaT细胞,分析细胞内自噬体水平。结果:在pm2.5处理的HaCaT细胞中,LBP预处理降低了pm2.5诱导的细胞毒性,改善了细胞形态,减少了细胞凋亡。LBP还能抑制GRP78和CHOP的表达水平,降低LC3I向LC3II的转化,抑制Bax蛋白,激活Bcl-2蛋白。此外,枸杞多糖可抑制pm2.5诱导的线粒体自噬(mitophagy)和线粒体损伤。pm2.5诱导的自噬受内质网应激的调节。结论:枸杞多糖通过调节氧化应激-内质网应激-自噬-凋亡信号轴保护皮肤细胞免受pm2.5诱导的细胞毒性,提示枸杞多糖具有一定的皮肤保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy.

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy.

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy.

Lycium Barbarum polysaccharide protects HaCaT cells from PM2.5-induced apoptosis via inhibiting oxidative stress, ER stress and autophagy.

Objectives: Lycium barbarum polysaccharide (LBP) is a natural polysaccharide extracted from Lycium barbarum that has anti-inflammatory, anti-apoptotic and anti-aging effects, and plays a role in the prevention and treatment of various diseases. In this study, we investigated the therapeutic effect of LBP on particulate matter 2.5 (PM2.5)-induced skin damage.Methods: Cell viability was analyzed by MTT and LDH assays. Apoptosis was analyzed by Annexin V-FITC/PI staining. Oxidative stress/damage were assessed by intracellular ROS levels, MDA content and SOD activity. The intracellular protein expression was analyzed by Western blot. Mitochondrial damage was assayed by mitochondrial membrane potential with JC-1 probe. LC3-GFP adenovirus was transfected into HaCaT cells to analyze intracellular autophagosome levels.Results: In PM2.5-treated HaCaT cells, LBP pretreatment reduced PM2.5-induced cytotoxicity, ameliorated cell morphology and reduced cell apoptosis. LBP also inhibited the expression levels of GRP78 and CHOP, reduced the conversion of LC3I to LC3II, inhibited Bax protein and activated Bcl-2 protein. Furthermore, LBP inhibited PM2.5-induced mitochondrial autophagy (mitophagy) and mitochondrial damage. PM2.5-induced autophagy was regulated by endoplasmic reticulum (ER) stress.Conclusion: LBP protects skin cells from PM2.5-induced cytotoxicity by regulating the oxidative stress-ER stress-autophagy-apoptosis signaling axis, revealing that LBP has a great potential for the skin protection.

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来源期刊
Redox Report
Redox Report 生物-生化与分子生物学
CiteScore
6.10
自引率
0.00%
发文量
28
审稿时长
>12 weeks
期刊介绍: Redox Report is a multidisciplinary peer-reviewed open access journal focusing on the role of free radicals, oxidative stress, activated oxygen, perioxidative and redox processes, primarily in the human environment and human pathology. Relevant papers on the animal and plant environment, biology and pathology will also be included. While emphasis is placed upon methodological and intellectual advances underpinned by new data, the journal offers scope for review, hypotheses, critiques and other forms of discussion.
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