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姜黄素对D-半乳糖诱导的LLC-PK1和HK-2细胞衰老及氧化应激的保护作用

Protective Effect of Curcumin on D-Galactose-Induced Senescence and Oxidative Stress in LLC-PK1 and HK-2 Cells.

作者信息

García-Trejo Semiramis Stephania, Gómez-Sierra Tania, Eugenio-Pérez Dianelena, Medina-Campos Omar Noel, Pedraza-Chaverri José

机构信息

Department of Biology, Faculty of Chemistry, National Autonomous University of Mexico (UNAM), Mexico City 04510, Mexico.

出版信息

Antioxidants (Basel). 2024 Mar 29;13(4):415. doi: 10.3390/antiox13040415.

DOI:10.3390/antiox13040415
PMID:38671863
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11047423/
Abstract

D-galactose has been widely used as an inducer of cellular senescence and pathophysiological processes related to aging because it induces oxidative stress. On the other hand, the consumption of antioxidants such as curcumin can be an effective strategy to prevent phenotypes related to the enhanced production of reactive oxygen species (ROS), such as aging and senescence. This study aimed to evaluate the potential protective effect of curcumin on senescence and oxidative stress and endoplasmic reticulum stress induced by D-galactose treatment in Lilly Laboratories Culture-Porcine Kidney 1 (LLC-PK1) and human kidney 2 (HK-2) proximal tubule cell lines from pig and human, respectively. For senescence induction, cells were treated with 300 mM D-galactose for 120 h and, to evaluate the protective effect of the antioxidant, cells were treated with 5 µM curcumin for 24 h and subsequently treated with curcumin + D-galactose for 120 h. In LLC-PK1 cells, curcumin treatment decreased by 20% the number of cells positive for senescence-associated (SA)-β-D-galactosidase staining and by 25% the expression of 8-hydroxy-2'-deoxyguanosine (8-OHdG) and increased by 40% lamin B1 expression. In HK-2 cells, curcumin treatment increased by 60% the expression of proliferating cell nuclear antigen (PCNA, 50% Klotho levels, and 175% catalase activity. In both cell lines, this antioxidant decreased the production of ROS (20% decrease for LLC-PK1 and 10 to 20% for HK-2). These data suggest that curcumin treatment has a moderate protective effect on D-galactose-induced senescence in LLC-PK1 and HK-2 cells.

摘要

D-半乳糖因其能诱导氧化应激,已被广泛用作细胞衰老及与衰老相关的病理生理过程的诱导剂。另一方面,食用姜黄素等抗氧化剂可能是预防与活性氧(ROS)生成增加相关表型(如衰老和细胞衰老)的有效策略。本研究旨在评估姜黄素对分别来自猪和人的Lilly Laboratories Culture-Porcine Kidney 1(LLC-PK1)和人肾2(HK-2)近端小管细胞系中由D-半乳糖处理诱导的细胞衰老、氧化应激和内质网应激的潜在保护作用。为诱导细胞衰老,细胞用300 mM D-半乳糖处理120小时,为评估抗氧化剂的保护作用,细胞先用5 μM姜黄素处理24小时,随后用姜黄素 + D-半乳糖处理120小时。在LLC-PK1细胞中,姜黄素处理使衰老相关(SA)-β-D-半乳糖苷酶染色阳性细胞数量减少20%,8-羟基-2'-脱氧鸟苷(8-OHdG)表达降低25%,核纤层蛋白B1表达增加40%。在HK-2细胞中,姜黄素处理使增殖细胞核抗原(PCNA)表达增加60%,Klotho水平增加50%,过氧化氢酶活性增加175%。在两种细胞系中,这种抗氧化剂均降低了ROS的产生(LLC-PK1细胞降低20%,HK-2细胞降低10%至20%)。这些数据表明,姜黄素处理对LLC-PK1和HK-2细胞中D-半乳糖诱导的衰老具有适度的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/eef765153791/antioxidants-13-00415-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/04ef8f73689a/antioxidants-13-00415-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/90ef91c68bbd/antioxidants-13-00415-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/c3bf589c4193/antioxidants-13-00415-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/ad5f51c5c9c2/antioxidants-13-00415-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/72872d317500/antioxidants-13-00415-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/27503dbe145a/antioxidants-13-00415-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/eef765153791/antioxidants-13-00415-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/04ef8f73689a/antioxidants-13-00415-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/c906030c2633/antioxidants-13-00415-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/90ef91c68bbd/antioxidants-13-00415-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/51ecfc27817f/antioxidants-13-00415-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/67e6aee919ee/antioxidants-13-00415-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/c3bf589c4193/antioxidants-13-00415-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/ad5f51c5c9c2/antioxidants-13-00415-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/72872d317500/antioxidants-13-00415-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/27503dbe145a/antioxidants-13-00415-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c165/11047423/eef765153791/antioxidants-13-00415-g010.jpg

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