A selenium polysaccharide from Platycodon grandiflorum rescues PC12 cell death caused by H 2 O 2 via inhibiting oxidative stress

In this paper, a selenium polysaccharide (PGP1) was isolated from the radix of Platycodon grandiflorum. We investigated the protective capacity of PGP1 against the hydrogen peroxide (H O )-induced oxidative damage in cultured rat pheochromocytoma (PC12) cells. Cells were pretreated with various dose...

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Bibliographic Details
Published in:International journal of biological macromolecules 2017-11, Vol.104 (Pt A), p.393
Main Authors: Sheng, Yu, Liu, Guangchen, Wang, Manli, Lv, Zuying, Du, Peige
Format: Article
Language:English
Subjects:
Animals
Apoptosis - drug effects
Cell Survival - drug effects
Hydrogen Peroxide - pharmacology
Malondialdehyde - metabolism
Oxidative Stress - drug effects
PC12 Cells
Platycodon - chemistry
Polysaccharides - chemistry
Polysaccharides - pharmacology
Rats
Selenium - chemistry
Superoxide Dismutase - metabolism
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Summary:In this paper, a selenium polysaccharide (PGP1) was isolated from the radix of Platycodon grandiflorum. We investigated the protective capacity of PGP1 against the hydrogen peroxide (H O )-induced oxidative damage in cultured rat pheochromocytoma (PC12) cells. Cells were pretreated with various doses of PGP1 (50, 100 and 200μg/mL) for 24h before exposure to 0.5mM H O for 12h. Cell viability, LDH release, apoptotic rates, malondialdehyde (MDA) content, antioxidant enzyme superoxide dismutase (SOD) activity and intracellular accumulation of reactive oxygen species (ROS) were determined. The results showed pretreatment of PC12 cells with PGP1 prior to H O exposure inhibited the decrease of cell viability, decreased the apoptotic rates, prevented membrane damage (LDH release) and attenuated intracellular ROS formation in PC12 cells injured by H O . Meanwhile, PGP1 increased SOD activity, while it decreased the level of MDA and the production of lipid peroxidation, in PC12 cells after H O exposure. These findings suggested that PGP1 may be considered as a potential useful antioxidant agent in reducing neuronal oxidative damage via inhibiting oxidative stress.
ISSN:1879-0003