Silibinin Protects against H2O2-Induced Oxidative Damage in SH-SY5Y Cells by Improving Mitochondrial Function

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 Silybum marianum, exhibits multiple biological activities. The present study investigated the effects of silibinin on H2O2-induced oxidative stress in human neuroblastoma SH-SY5Y cells. Exposure to H2O2 (750 µM) 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 H2O2-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 H2O2-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.

Silybin Alleviated Hepatic Injury by Regulating Redox Balance, Inflammatory Response, and Mitochondrial Function in Weaned Piglets under Paraquat-Induced Oxidative Stress

“…Conversely, silybin supplementation markedly normalizes mitochondrial dynamic imbalance under PQ challenge. An in vitro study also suggested that silybin treatment protects human neuroblastoma SH-SY5Y cells from H 2 O 2 -induced mitochondrial damage by regulating OPA1 and Drp1 protein expression [ 57 ]. Collectively, silybin supplementation protected against PQ-induced liver injury in piglets by improving mitochondrial functions.…”

Kaempferol Derivatives from Hippophae rhamnoides Linn. Ameliorate H2O2‐Induced Oxidative Stress in SH‐SY5Y Cells by Upregulating Nrf2

“…The pharmacological activity associated with flavonoids in H. rhamnoides encompasses antioxidant, hypoglycemic, hypolipidemic, and antitumor effects. [13,14,26] The current study aimed to isolate and characterize three new kaempferol derivatives from the seed residue of H. rhamnoides, a plant that is regarded as industrial waste. These derivatives each incorporate four sugar moieties that share the core nuclear structure of kaempferol, which is essential for their antioxidative potential.…”

Modulation of cytotoxic amyloid fibrillation and mitochondrial damage of α-synuclein by catechols mediated conformational changes

“…The SH-SY5Y cells were cultured in 6-well dishes at 5 × 10 5 cells/well density and incubated overnight. Then, cells were treated with 20 µM incubated samples aged alone or in the presence of 200 µM catechols and incubated for 6 h. Cells treated with 750 µM H 2 O 2 70 were used as a positive control. After incubation, 5 µM DCFDA was added to each Petri dish, and cells were incubated for an additional 30 min at 37 °C.…”