Abstract: Objective LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Methods LPS-treated PC12 cells were used to establish neuron inflammation model. RT-PCR was used to detect the mRNA of cytokines. CCK-8 assay was used to check determine cell viability. Western blot was used to detect NF-κB pathway. Results After 12 hrs treatment of PC12 cells with different doses of LPS (0, 100, 300 and 1 000 ng/mL), the mRNA level of TNF-α,IL-6 and IL-1β all increased. The cells pre-treated with different doses of gypenoside (30, 100 μg/mL) and then treated with LPS for 24 h, cell viability decreased to 85.7%. However, 30 and 100 μg/mL gypenoside pre-treatment resulted in cell viability increased to 96.2% and 97.9% respectively. Gypenoside also inhibited LPS-induced cell inflammation as indicated by increased mRNA level of TNF-α, IL-6 and IL-1β caused by LPS stimulation. LPS increased the phosphorylation of p65 (p-p65) and the phosporylation was also inhibited by gypenoside treatment. Conclusions Gypenoside alleviates LPS-induced inflammation and then protects PC12 cells from injury induced by LPS through inhibiting NF-κB pathway.

Key words: gypenoside, inflammation, lipopolysaccharide (LPS), PC12 cells