Combining antioxidant astaxantin and cholinesterase inhibitor huperzine A boosts neuroprotection
| Autor: | Han‑Mei Wei, Hong Nie, Chang‑Jian Li, Zi‑Jun Zhao, Jun Zhao, He‑Kun Zeng, Xin Yang, Li‑Na Long, Guo‑Yan Hu |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cancer Research Xanthophylls Pharmacology medicine.disease_cause Biochemistry Neuroprotection Antioxidants Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound Alkaloids 0302 clinical medicine Alzheimer Disease Genetics medicine Animals Viability assay Molecular Biology Huperzine A chemistry.chemical_classification Reactive oxygen species biology Neurotoxicity PC12 cells huperzine A neuroprotective Articles Malondialdehyde medicine.disease Rats astaxanthin Oxidative Stress Neuroprotective Agents 030104 developmental biology Oncology chemistry 030220 oncology & carcinogenesis biology.protein Molecular Medicine Cholinesterase Inhibitors Sesquiterpenes Oxidative stress medicine.drug |
| Zdroj: | Molecular Medicine Reports |
| ISSN: | 1791-3004 1791-2997 |
| DOI: | 10.3892/mmr.2020.10920 |
| Popis: | 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, Aβ25‑35, 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 Aβ25‑35. 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. |
| Databáze: | OpenAIRE |
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