The Research On The Protective Function Of Gastrodine To The Oxidative Stress Injury Induced By LPS In PC12Cells

Objective The purpose of this research was to investigate the protective function of gastrodin in the lipopolysaccharide (LPS) induced to produce oxidative stress injury model of PC12cells (the mouse adrenal gland pheochromocytoma cells).Methods PC12cells were cultured and treated in different time in vitro. During the experiments, PC12cells were randomly divided into three groups, including the blank control group, the LPS treatment group (the model group) and the LPS plus gastrodine treatment group. In treatment groups, quantification of cell death and changes in morphology were observed by using Hoechst33342/PI nuclear staining and fluorescence microscopy. Intracelluar ROS were measured by using the fluorescent probe, H2DCFDA, with spectrofluoro-photometer.Results In this research, we successfully set up the oxidative stress PC12cell model induced by LPS. When the optimal concentration and time of LPS is200ng/ml and1h, the production of intracelluar ROS was increased obviously (P<0.05), and the number of cell death is the highest (P<0.05). The production of intracelluar ROS in PC12cells was inhibited by gastrodin in a concentration-dependent manner, especially when the concentration of gastrodin is20μmol/L. More strikingly,20μmol/L gastrodin could inhibit LPS-induced apoptosis and necrosis obviously (P<0.05).Conclusions PC12cells is one of the most commonly used cellular model of oxidative stress injury. They are used as well vitro cell model of Alzheimer's disease, because that they have sympathetic neurons features at the same time. LPS could induce the increase of intracelluar ROS and the number of necrosis in PC12cells. Gastrodine had obvious role in protection and could suppress LPS-induced necrosis of cells. Arising from the above, we suggest that gastrodin has a potential as an anti-oxidative stress drug candidate in therapy of Alzheimer's disease.