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探索纳米氧化铈保护HT22细胞免受氧化应激的抗氧化机制。

Exploring the Antioxidant Mechanisms of Nanoceria in Protecting HT22 Cells from Oxidative Stress.

作者信息

Dong Da-Long, Jin Guang-Zhen

机构信息

Institute of Tissue Regeneration Engineering (ITREN), Dankook University, Cheonan 31116, Republic of Korea.

Department of Nanobiomedical Science and BK21 PLUS NBM Global Research Center for Regenerative Medicine, Dankook University, Cheonan 31116, Republic of Korea.

出版信息

Int J Mol Sci. 2024 Dec 11;25(24):13281. doi: 10.3390/ijms252413281.

DOI:10.3390/ijms252413281
PMID:39769046
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11675852/
Abstract

An excess of reactive oxygen species (ROS), leading to oxidative stress, is a major factor in aging. Antioxidant therapies are considered crucial for delaying aging. Nanoceria, a nanozyme with antioxidant activity, holds significant potential in protecting cells from oxidative stress-induced damage. This research examines the neuroprotective role of nanoceria on HT22 cells subjected to oxidative stress induced by hydrogen peroxide (HO) and explores the associated molecular mechanisms. Our findings indicate that nanoceria enhances bcl-2 expression and significantly reduces Bax expression, resulting in an increased bcl-2/Bax ratio, which confirms its anti-apoptotic effect. Nanoceria boosts catalase expression and suppresses the p38 MAPK signaling pathway, indicating its role in shielding HT22 cells from oxidative stress damage induced by HO through various protective mechanisms. These findings provide crucial experimental evidence for the potential applications of nanoceria in skin anti-aging and the prevention and treatment of other oxidative stress-related diseases.

摘要

过量的活性氧(ROS)会导致氧化应激,是衰老的一个主要因素。抗氧化疗法被认为对延缓衰老至关重要。纳米氧化铈是一种具有抗氧化活性的纳米酶,在保护细胞免受氧化应激诱导的损伤方面具有巨大潜力。本研究考察了纳米氧化铈对过氧化氢(H₂O₂)诱导的氧化应激作用下HT22细胞的神经保护作用,并探讨了相关分子机制。我们的研究结果表明,纳米氧化铈可增强bcl-2表达并显著降低Bax表达,导致bcl-2/Bax比值升高,证实了其抗凋亡作用。纳米氧化铈可提高过氧化氢酶表达并抑制p38 MAPK信号通路,表明其通过多种保护机制在保护HT22细胞免受H₂O₂诱导的氧化应激损伤中发挥作用。这些研究结果为纳米氧化铈在皮肤抗衰及其他氧化应激相关疾病防治中的潜在应用提供了关键实验证据。

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