BACKGROUND: Astrocytes participate in central nervous system-mediated physiological or pathological processes, such as pain. Activated dorsal horn astrocytes from the spinal cord produce nerve active substances and proinflammatory cytokines, such as interleukin-I beta (IL-1 β ), IL-6, and tumor necrosis factor-a (TNF-a ), which play important roles in pain transduction and regulation. OBJECTIVE: To investigate the effects of different doses of propofol on activation of cultured spinal cord dorsal horn astrocytes induced by glutamate, as well as changes in IL-1 β, IL-6, and TNF-a, and IL-10 (anti-inflammatory cytokine) expression in rats, and to explore the dose relationship of propofnl. DESIGN, TIME AND SETTING: The cellular and molecular biology experiment was performed at the Central Laboratory of Yunyang Medical College between March 2006 and December 2007. MATERIALS: Forty healthy, Wistar rats, aged 2-3 days, were selected. Propofol was provided by Zeneca, UK; glutamate by Sigma, USA; EPICS XL flow cytometry by Beckman culture, USA; rabbit-anti-mouse glial fibrillary acidic protein (GFAP) antibody kit and inflammatory cytokine detection kit were provided by Zhongshan Biotechnology Company Ltd., Beijing; multimedia color pathologic image analysis system was a product of Nikon, Japan. METHODS: Astrocytes were harvested from T11-L6spinal cord dorsal horn of Wistar rats and incubated for 3 weeks. The cells were divided into seven groups, according to various treatment conditions: control group was cells cultured in Hank's buffered saline solution; intralipid group was cells cultured in intralipid (0.2 mL/L); glutamate group was cells cultured with 100 μ mol/L glutamate; propofol group was cells cultured with 250 μ mol/L propofol; three glutamate plus propofol groups were cultured in 100 μ mol/L of glutamate, followed by 5, 25, and 250 μ mol/L of prnpofol 10 minutes later. MAIN OUTCOME MEASURES: GFAP-labeled astrocytes were analyzed using a multimedia pathology imaging analysis system to detect area density (AD) and average optical density (AOD) of positive cells. The supernatant concentrations of IL-1 β, TNF- a, IL-6, and IL-10 were determined using radioimmune assays. RESULTS: Compared with the control group, cells in the glutamate plus low-dose propofol group were activated and hypertrophic, and AD and AOD were significantly increased (P < 0.01 ). Concentrations of IL-1 β, TNF- a, and IL-6 were also significantly increased (P < 0.01 ), while IL-10 levels remained unchanged (P > 0.05), but still higher than the control and glutamate groups (P>0.05). Compared with the glutamate group, astrocyte activation was inhibited by moderate and high-dose propofol. In addition, with moderate and high-dose propofol, AD, AOD, IL-1 β, TNF-a, and IL-6 concentrations were significantly decreased (P < 0.05-0.01 ), and IL-10 levels were increased (P < 0.01 ). CONCLUSION: Propofol can effectively inhibit glutamate-induced astrocyte activation in the spinal cord dorsal horn, significantly inhibit production of IL-1β, TNF-a, and IL-6, and increase IL- 10 synthesis and release in a dose-dependent manner.