Objective: To observe the effect of scutellarin(Scu) on expression of several inflammatory factors in the brains of rats with dementia and to reveal the possible therapeutic mechanism on dementia. Method: Wistar rats were randomly divided into 5 groups

ie

normal

sham operation

learning and memory deficit model

Scu treatment and piracetam treatment groups. The rat dementia model was produced by bilateral ventricle injection with β-amyloid peptide (Aβ25-35) and abdominal cavity injection with D-galactose. The rats in Scu or piracetam group were treated with 28 mg·kg-1 and 365 mg·kg-1 of 0.5% Scu or 64 g·L-1 piracetam by intragastric gavage (ig) for 20 days after modeling. NF-κB p65 at mRNA levels were detected by real-time PCR

and the expressions of interleukin-1β(IL-1β)

interleukin-6 (IL-6) and tumor necrosis factor-α(TNF-α) were observed by immunohistochemistry method in the brain of rats. Result: As compared to normal or sham operation groups

NF-κB p65 mRNA expression in the model group was up-regulated by 27% and 31%

the expressions of IL-1β

IL-6 and TNF-α were increased from 1.3±0.48

1.6±0.52

1.6±0.69 and 1.5±0.53

1.6±0.70

2.0±0.67 to 2.9±0.74

3.2±0.79

3.0±0.82(P<0.05). After treatment by Scu

NF-κB p65 mRNA expression were down-regulated by 20% (P<0.05) and scores of positive cells of IL-1β

IL-6 and TNF-α were respectively decreased by 2.1±0.67

2.3±0.70

2.2±0.53 (P<0.05) in brain tissues as compared to learning and memory deficit group. Conclusion: By preventing activation of NF-κB p65 and inhibiting releasing of mediators of inflammation

Scu may be able to improve the ability of learning and memory of the rats with dementia and to educe neuroprotective effects.