Article Publish Status: FREE
Abstract Title:

Neuroprotective Effects ofon Stress-Induced Hippocampal Deficits in Rats and HO-Induced Neurotoxicity in SH-SY5Y Neuroblastoma Cells.

Abstract Source:

Antioxidants (Basel). 2019 Dec 26 ;9(1). Epub 2019 Dec 26. PMID: 31888114

Abstract Author(s):

Weishun Tian, Jing Zhao, Jeong-Ho Lee, Md Rashedunnabi Akanda, Jeong-Hwi Cho, Sang-Ki Kim, Yu-Jin Choi, Byung-Yong Park

Article Affiliation:

Weishun Tian


Oxidative stress plays a vital role in neurodegenerative diseases.(CC) has a wide range of pharmacological activities (e.g., antioxidant, neuroprotective, and anti-inflammatory). The present study was undertaken to elucidate the neuroprotective mechanism of CC and fermented CC (FCC) on stress and HO-induced oxidative stress damage in rats and SH-SY5Y cells. A dose of 100 mg/kg CC or FCC was orally administered to rats 1 h prior to immobilization 2 h per day for 14 days. CC, especially FCC administration decreased immobility time in forced swim test (FST), effectively alleviated the oxidative stress, and remarkably decreased corticosterone,β-endorphin and increased serotonin levels, respectively. In cells, CC and FCC significantly inhibited reactive oxygen species (ROS) generation, lactate dehydrogenase (LDH) release and significantly increased the genes expression of antioxidant and neuronal markers, such as superoxide dismutase (SOD), catalase (CAT), and brain-derived neurotrophic factor (BDNF). Moreover, the pro-apoptotic factor Bax and anti-apoptotic factor Bcl-2 (Bax/Bcl-2) ratio was regulated by CC and FCC pretreatment. Both in rats and cells, CC and FCC downregulated mitogen-activated protein kinase (MAPK) phosphorylation. Taken together, these results demonstrated that CC and particularly FCC ameliorated oxidative stress and may be used on the neuroprotection.

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