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KGF-2 通过 Akt/Nrf2/HO-1 通路对人晶状体上皮细胞氧化应激损伤和细胞凋亡的保护作用。

Protection of Human Lens Epithelial Cells from Oxidative Stress Damage and Cell Apoptosis by KGF-2 through the Akt/Nrf2/HO-1 Pathway.

机构信息

Department of Ophthalmology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou 325000, China.

School of Pharmaceutical Science, Wenzhou Medical University, Wenzhou 325000, China.

出版信息

Oxid Med Cell Longev. 2022 Feb 17;2022:6933812. doi: 10.1155/2022/6933812. eCollection 2022.

DOI:10.1155/2022/6933812
PMID:35222803
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8872674/
Abstract

Oxidative stress exerts a significant influence on the pathogenesis of various cataracts by inducing degradation and aggregation of lens proteins and apoptosis of lens epithelial cells. Keratinocyte growth factor-2 (KGF-2) exerts a favorable cytoprotective effect against oxidative stress and . In this work, we investigated the molecular mechanisms of KGF-2 against hydrogen peroxide- (HO-) induced oxidative stress and apoptosis in human lens epithelial cells (HLECs) and rat lenses. KGF-2 pretreatment could reduce HO-induced cytotoxicity as well as reactive oxygen species (ROS) accumulation. KGF-2 also increases B-cell lymphoma-2 (Bcl-2), quinine oxidoreductase-1 (NQO-1), superoxide dismutase (SOD2), and catalase (CAT) levels while decreasing the expression level of Bcl2-associated X (Bax) and cleaved caspase-3 in HO-stimulated HLECs. LY294002, the phosphatidylinositol-3-kinase (PI3K)/Akt inhibitor, abolished KGF-2's effect to some extent, demonstrating that KGF-2 protected HLECs via the PI3K/Akt pathway. On the other hand, KGF-2 activated the Nrf2/HO-1 pathway by regulating the PI3K/Akt pathway. Silencing nuclear factor erythroid 2-related factor 2 (Nrf2) by targeted-siRNA and inhibiting heme oxygenase-1 (HO-1) through zinc protoporphyrin IX (ZnPP) significantly decreased cytoprotection of KGF-2. Furthermore, as revealed by lens organ culture assays, KGF-2 treatment decreased HO-induced lens opacity in a concentration-dependent manner. As demonstrated by these data, KGF-2 resisted HO-mediated apoptosis and oxidative stress in HLECs through Nrf2/HO-1 and PI3K/Akt pathways, suggesting a potential protective effect against the formation of cataracts.

摘要

氧化应激通过诱导晶状体蛋白降解和聚集以及晶状体上皮细胞凋亡，对各种白内障的发病机制产生重大影响。角质细胞生长因子-2（KGF-2）对氧化应激具有良好的细胞保护作用，并能。在这项工作中，我们研究了 KGF-2 对人晶状体上皮细胞（HLECs）和大鼠晶状体中过氧化氢（HO-）诱导的氧化应激和细胞凋亡的分子机制。KGF-2 预处理可降低 HO 诱导的细胞毒性和活性氧（ROS）积累。KGF-2 还增加 B 细胞淋巴瘤-2（Bcl-2）、醌氧化还原酶-1（NQO-1）、超氧化物歧化酶（SOD2）和过氧化氢酶（CAT）的水平，同时降低 HO 刺激的 HLECs 中 Bcl2 相关 X（Bax）和裂解 caspase-3 的表达水平。PI3K/Akt 抑制剂 LY294002 在一定程度上消除了 KGF-2 的作用，表明 KGF-2 通过 PI3K/Akt 途径保护 HLECs。另一方面，KGF-2 通过调节 PI3K/Akt 通路激活 Nrf2/HO-1 通路。通过靶向-siRNA 沉默核因子红细胞 2 相关因子 2（Nrf2）并通过锌原卟啉 IX（ZnPP）抑制血红素加氧酶-1（HO-1）显著降低了 KGF-2 的细胞保护作用。此外，晶状体器官培养实验表明，KGF-2 以浓度依赖的方式降低 HO 诱导的晶状体混浊。这些数据表明，KGF-2 通过 Nrf2/HO-1 和 PI3K/Akt 通路抵抗 HO 介导的 HLECs 凋亡和氧化应激，提示其对白内障形成具有潜在的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/b7e4d2b022ba/OMCL2022-6933812.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/f93c2726b6ed/OMCL2022-6933812.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/f38970aeab2a/OMCL2022-6933812.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/b734ff949575/OMCL2022-6933812.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/c8ff6937ceaf/OMCL2022-6933812.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/c31a57f6e9c0/OMCL2022-6933812.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/b7e4d2b022ba/OMCL2022-6933812.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/f93c2726b6ed/OMCL2022-6933812.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/f38970aeab2a/OMCL2022-6933812.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/b734ff949575/OMCL2022-6933812.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/c8ff6937ceaf/OMCL2022-6933812.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/c31a57f6e9c0/OMCL2022-6933812.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9d7b/8872674/b7e4d2b022ba/OMCL2022-6933812.006.jpg

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