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Article Publish Status: FREE
Abstract Title:

Silibinin Protects against HO-Induced Oxidative Damage in SH-SY5Y Cells by Improving Mitochondrial Function.

Abstract Source:

Antioxidants (Basel). 2022 May 31 ;11(6). Epub 2022 May 31. PMID: 35739997

Abstract Author(s):

Fangfang Tie, Yangyang Fu, Na Hu, Honglun Wang

Article Affiliation:

Fangfang Tie

Abstract:

Oxidative stress plays a critical role in the pathogenesis of various neurodegenerative diseases. Increasing evidence suggests the association of mitochondrial abnormalities with oxidative stress-related neural damage. Silibinin, a natural flavonol compound isolated from, exhibits multiple biological activities. The present study investigated the effects of silibinin on HO-induced oxidative stress in human neuroblastoma SH-SY5Y cells. Exposure to HO(750µM) reduced the viability of SH-SY5Y cells, which was coupled with increased reactive oxygen species (ROS), abnormal cell morphology, and mitochondrial dysfunction. Remarkably, silibinin (1, 5, and 10 µM) treatment attenuated the HO-induced cell death. Moreover, silibinin reduced ROS production and the levels of malondialdehyde (MDA), increased the levels of superoxide dismutase (SOD) and glutathione (GSH), and increased mitochondrial membrane potential. Moreover, silibinin normalized the expression of nuclear factor 2-related factor 2 (Nrf2)-related and mitochondria-associated proteins. Taken together, our findings demonstrated that silibinin could attenuate HO-induced oxidative stress by regulating Nrf2 signaling and improving mitochondrial function in SH-SY5Y cells. The protective effect against oxidative stress suggests silibinin as a potential candidate for preventing neurodegeneration.

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