College of Pharmacy, Beihua University, Jilin 132013, China.
Department of Orthopaedic Trauma, The First Bethune Hospital of Jilin University, Changchun 130021, China.
Int J Biol Macromol. 2017 Nov;104(Pt A):393-399. doi: 10.1016/j.ijbiomac.2017.06.052. Epub 2017 Jun 10.
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 (HO)-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 HO 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 HO 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 HO. Meanwhile, PGP1 increased SOD activity, while it decreased the level of MDA and the production of lipid peroxidation, in PC12 cells after HO exposure. These findings suggested that PGP1 may be considered as a potential useful antioxidant agent in reducing neuronal oxidative damage via inhibiting oxidative stress.
本文从桔梗中分离得到一种硒多糖(PGP1)。我们研究了 PGP1 对过氧化氢(HO)诱导的培养大鼠嗜铬细胞瘤(PC12)细胞氧化损伤的保护作用。细胞在暴露于 0.5mM HO 12h 之前用不同剂量的 PGP1(50、100 和 200μg/mL)预处理 24h。测定细胞活力、LDH 释放、凋亡率、丙二醛(MDA)含量、抗氧化酶超氧化物歧化酶(SOD)活性和细胞内活性氧(ROS)的积累。结果表明,HO 暴露前用 PGP1 预处理 PC12 细胞可抑制细胞活力下降,降低凋亡率,防止膜损伤(LDH 释放),减轻 HO 损伤的 PC12 细胞内 ROS 的形成。同时,PGP1 增加了 SOD 活性,降低了 MDA 水平和脂质过氧化产物的产生,在 HO 暴露后的 PC12 细胞中。这些发现表明,PGP1 可通过抑制氧化应激,被视为一种潜在的有用的抗氧化剂,减少神经元氧化损伤。