Microsomal glutathione transferase 1 attenuated ROS-induced lipid peroxidation in Apostichopus japonicus

Zhang, Zhen; Lv, Zhimeng; Shao, Yina; Qiu, Qiongfen; Zhang, Weiwei; Duan, Xuemei; Li, Ye; Li, Chenghua

doi:10.1016/j.dci.2017.03.011

Cited by 14 publications

(12 citation statements)

References 45 publications

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“…6B), the cell viability in the 250 µM group was still higher than in the 500 µM group. So, 250 µM was chosen as the optimal dose in the aβ [25][26][27][28][29][30][31][32][33][34][35] -induced Pc12 cell model study.…”

Section: Resultsmentioning

confidence: 99%

“…Chemicals. Hupa and aXT (>98% in purity) were purchased from Sichuan Weikeqi Biological Technology co., ltd. TBHP solution was purchased from Shanghai Macklin Biochemical Co., Ltd. Dulbecco's modified Eagle's medium (dMeM), fetal bovine serum (FBS) and 0.25% (w/v) trypsin solution were purchased from Gibco; Thermo Fisher Scientific, inc. aβ [25][26][27][28][29][30][31][32][33][34][35] was purchased from BioSS. MTT and 2,7'-dichlorodihydrofluorescein diacetate (DCFH-DA) were purchased from Sigma-aldrich; Merck KGaa.…”

Section: Methodsmentioning

confidence: 99%

“…Ah [25][26][27][28][29][30][31][32][33][34][35] -induced cell injury. aβ [25][26][27][28][29][30][31][32][33][34][35] was dissolved in sterilized PBS at a concentration of 1 mM and incubated for 7 days at 37˚C for aggregation. The solution was diluted in culture medium prior to each experiment.…”

Section: Methodsmentioning

confidence: 99%

“…The solution was diluted in culture medium prior to each experiment. Pc12 cells were seeded in 96-well plates at a density of 5x10 3 cells/well for 24 h. Then, cells were incubated with different concentrations (5, 10, 20 and 40 µM) of aβ [25][26][27][28][29][30][31][32][33][34][35] for 24 h at 37˚C. Subsequently, MTT (20 µl) solution (5 mg/ml) was added to each well for 4 h at 37˚C.…”

Section: Methodsmentioning

confidence: 99%

“…Pc12 cells were cultured on 96-well plates and pretreated with Hupa (0.625, 6.25, 62.5, 125, 250 and 500 µM) or aXT (0.01, 0.1, 1 and 10 µM) for 24 h before the introduction of aβ [25][26][27][28][29][30][31][32][33][34][35] (20 µM). cell viability was determined using an MTT assay.…”

Section: Methodsmentioning

confidence: 99%

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Combining antioxidant astaxantin and cholinesterase inhibitor huperzine A boosts neuroprotection

Yang

Wei

et al. 2020

Mol Med Report

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oxidative stress is a pathophysiological condition resulting in neurotoxicity, which is possibly associated with neurodegenerative disorders. in this study, the antioxidative effects of the antioxidant astaxanthin (aXT) in combination with huperzine a (Hupa), which is used as a cholinesterase inhibitor for the treatment of alzheimer's disease, were investigated. Pc12 cells were treated with either tert-butyl hydroperoxide (TBHP), or with the toxic version of β-amyloid, aβ 25-35 , to induce oxidative stress and neurotoxicity. cell viability, morphology, lactate dehydrogenase (ldH) release, intracellular accumulation of reactive oxygen species (roS), superoxide dismutase (Sod) activity and malondialdehyde (Mda) content were determined, while neuroprotection was also monitored using an MTT assay. it was found that combining AXT with HupA significantly increased the viability of PC12 cells, prevented membrane damage (as measured by ldH release), attenuated intracellular roS formation, increased Sod activity and decreased the level of Mda after TBHP exposure when compared to these drugs administered alone. Pretreatment with Hupa and aXT decreased toxic damage produced by aβ 25-35. These data indicated that combining an antioxidant with a cholinesterase inhibitor increases the degree of neuroprotection; with future investigation this could be a potential therapy used to decrease neurotoxicity in the brain.

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