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Neolitsea sericea attenuates oxidative stress-induced cell death in human neuroblastoma SH-SY5Y cells via MAPK and NF-κB pathway Inhibition
被引:0
作者:
Shin, Mi Song
[1
]
Song, Parkyong
[2
]
Choi, Seo Young
[1
]
Lee, You Kyeong
[1
]
Hwang, Ji Sun
[3
]
Son, Hong-Joo
[1
]
Kim, Yu-Jin
[1
]
Kim, Wanil
[4
,5
]
Lee, Kwang Min
[1
]
机构:
[1] Pusan Natl Univ, Dept Life Sci & Environm Biochem, Miryang 50463, South Korea
[2] Pusan Natl Univ, Dept Convergence Med, Sch Med, Yangsan 50612, South Korea
[3] Daegu Gyeongbuk Med Innovat Fdn, New Drug Dev Ctr, Daegu 41061, South Korea
[4] Gyeongsang Natl Univ, Dept Biochem, Dept Convergence Med Sci, Coll Med, Jinju 52727, South Korea
[5] Gyeongsang Natl Univ Coll Med, Inst Med Sci, Jinju 52727, South Korea
关键词:
Neolitsea sericea;
Hydrogen peroxide;
Oxidative stress;
Cell damage;
Apoptosis;
Neuronal cell death;
PARKINSONS-DISEASE;
METABOLISM;
DAMAGE;
ALPHA;
D O I:
10.1007/s11033-025-10682-1
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
BackgroundOxidative stress is a key contributor to the pathological mechanisms that underpin various neurodegenerative diseases. Hydrogen peroxide (H2O2) 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 resultsSH-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 NF kappa B transcription factors, indicating an anti-inflammatory effect.ConclusionsThese 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.
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