Objective To explore the neuroprotective mechanism of propofol by comparing the influence of propofol and isoflurane on inflammatory cytokines ( TNF-α、IL-1、ICAM-1 ) in patients with intracranial tumors. Methods One hundred and sixty-eight patients with intracranial neoplasm were randomly divided into two groups:the propofol ( Group P) and isoflurane (Group I),84 cases in each. Patients were given with propofol (3-6 μg·mL-1) by plasma target-controlled infusion or with continuously inhaled isoflurane ( 1%-2%) , respectively. The serum levels of TNF-α, IL-1 and ICAM-1 were detected before anesthesia and at 0,24,and 48 h after operation. Results The serum levels of TNF-α,IL-1 and ICAM-1 were significantly increased after operation as compared to baseline in both groups. The serum level of TNF-α was(69. 11±8. 95) and (76. 26±11.28) μg·mL-1,IL-1 was(21.57±3.19) and (29.58±4.38) ng·L-1,and ICAM-1 was (1.63±0.24)and (1.94±0.29) g·L-1 at 24 h post operation in Group P and Group I,respectively. These inflammatory cytokine levels were significantly higher in group I compared to group P at 24 and 48 h after operation (P<0. 05 or P<0. 01). Conclusion The target-controlled infusion of propofol brings about lower level of inflammatory reaction than isoflurane inhalation in patients with intracranial neoplasm,which may attribute to the mechanism of brain protection against injury.

Objective:This study aimed to explore the effects of trichosanthin on the proliferative inhibition and apoptosis induc-tion in human lung carcinoma A549 cells. Methods:A549 cells were treated with various concentrations of TCS. The inhibitory effects in proliferation were detected by the MTT method. The microfilament changes were observed by transmission electron microscopy. Apoptosis rate and cell cycle were determined by flow cytometry. Results:A549 cells treated with TCS presented apoptotic changes and decreased cell activity. When the concentration increased and time was prolonged, the inhibition rate increased correspondingly. Conclusion:Pharmacological doses of TCS inhibited the proliferation and differentiation in lung carcinoma A549 cells and affected the function in A549 cells by changes in the cytoskeleton.