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新木姜子通过抑制MAPK和NF-κB途径减轻氧化应激诱导的人神经母细胞瘤SH-SY5Y细胞死亡。

Neolitsea sericea attenuates oxidative stress-induced cell death in human neuroblastoma SH-SY5Y cells via MAPK and NF-κB pathway Inhibition.

作者信息

Shin Mi Song, Song Parkyong, Choi Seo Young, Lee You Kyeong, Hwang Ji Sun, Son Hong-Joo, Kim Yu-Jin, Kim Wanil, Lee Kwang Min

机构信息

Department of Life Science and Environmental Biochemistry, Pusan National University, Miryang, 50463, Republic of Korea.

Department of Convergence Medicine, Pusan National University School of Medicine, Yangsan, 50612, Republic of Korea.

出版信息

Mol Biol Rep. 2025 Jun 7;52(1):567. doi: 10.1007/s11033-025-10682-1.

Abstract

BACKGROUND

Oxidative stress is a key contributor to the pathological mechanisms that underpin various neurodegenerative diseases. Hydrogen peroxide (HO) is a well-known inducer of oxidative stress, which produces highly reactive hydroxyl radicals, resulting in cellular injury. The identification of bioactive compounds with potential neuroprotective properties is crucial for the development of novel therapeutic strategies. This study aimed to investigate the neuroprotective effects of Neolitsea sericea extract (NSE) in human SH-SY5Y neuroblastoma cells exposed to oxidative stress, as well as to understand the molecular mechanisms underlying these effects.

METHODS AND RESULTS

SH-SY5Y cells were pretreated with NSE before exposure to hydrogen peroxide (H₂O₂), and cell viability was assessed using a WST-1 assay. Western blotting was used to analyze key proteins involved in apoptosis and inflammatory signaling. NSE significantly decreased hydrogen peroxide (H₂O₂)-induced cytotoxicity in SH-SY5Y cells. NSE inhibited caspase-3 activation, regulated apoptosis-related protein expression by upregulating Bcl-2 and downregulating Bax, and suppressed the activation of mitogen-activated protein kinases. NSE also attenuated the nuclear translocation of NFκB transcription factors, indicating an anti-inflammatory effect.

CONCLUSIONS

These findings show that NSE effectively mitigates oxidative damage in neuronal cells, highlighting its potential as a complementary or alternative therapeutic method for the prevention and management of neurodegenerative diseases.

摘要

背景

氧化应激是多种神经退行性疾病病理机制的关键促成因素。过氧化氢(H₂O₂)是一种众所周知的氧化应激诱导剂,它会产生高活性的羟基自由基,导致细胞损伤。鉴定具有潜在神经保护特性的生物活性化合物对于开发新型治疗策略至关重要。本研究旨在探讨新樟提取物(NSE)对暴露于氧化应激的人SH-SY5Y神经母细胞瘤细胞的神经保护作用,并了解这些作用背后的分子机制。

方法与结果

在暴露于过氧化氢(H₂O₂)之前,用NSE预处理SH-SY5Y细胞,并使用WST-1测定法评估细胞活力。蛋白质印迹法用于分析参与凋亡和炎症信号传导的关键蛋白。NSE显著降低了过氧化氢(H₂O₂)诱导的SH-SY5Y细胞的细胞毒性。NSE抑制了半胱天冬酶-3的激活,通过上调Bcl-2和下调Bax来调节凋亡相关蛋白的表达,并抑制丝裂原活化蛋白激酶的激活。NSE还减弱了NFκB转录因子的核转位,表明具有抗炎作用。

结论

这些发现表明,NSE有效地减轻了神经元细胞中的氧化损伤,突出了其作为预防和管理神经退行性疾病的补充或替代治疗方法的潜力。

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