OBJECTIVE: To investigate the antioxidant and anti-endotoxin effects of propofol on endothelial cells and the possible mechanisms. METHODS: Cultured endothelial cells were treated with hydrogen peroxide (H(2)O(2)), propofol + H(2)O(2), lipopolysaccharide (LPS) and propofol + LPS, respectively. Endothelial cell damage was monitored for possible lactic dehydrogenase (LDH) release. The transcription and the protein expression levels of endothelial nitric oxide synthase (eNOS) were measured. RESULTS: LDH release was higher in groups treated with H(2)O(2) or LPS than in the control group. After pretreatment with propofol, the effects induced by H(2)O(2) were attenuated, but propofol did not decrease the LDH release induced by LPS. Both H(2)O(2) and LPS significantly increased the eNOS transcript levels and the increases were significantly attenuated after pretreatment with propofol. Both H(2)O(2) and LPS significantly increased the eNOS protein expression and the increase was attenuated after pretreatment with propofol. CONCLUSION: Propofol could protect endothelial cells against oxidative stress by inhibiting eNOS transcription and protein expression, but could not antagonise endotoxin induced cell injuries.
OBJECTIVE: To investigate the antioxidant and anti-endotoxin effects of propofol on endothelial cells and the possible mechanisms. METHODS: Cultured endothelial cells were treated with hydrogen peroxide (H(2)O(2)), propofol + H(2)O(2), lipopolysaccharide (LPS) and propofol + LPS, respectively. Endothelial cell damage was monitored for possible lactic dehydrogenase (LDH) release. The transcription and the protein expression levels of endothelial nitric oxide synthase (eNOS) were measured. RESULTS: LDH release was higher in groups treated with H(2)O(2) or LPS than in the control group. After pretreatment with propofol, the effects induced by H(2)O(2) were attenuated, but propofol did not decrease the LDH release induced by LPS. Both H(2)O(2) and LPS significantly increased the eNOS transcript levels and the increases were significantly attenuated after pretreatment with propofol. Both H(2)O(2) and LPS significantly increased the eNOS protein expression and the increase was attenuated after pretreatment with propofol. CONCLUSION:Propofol could protect endothelial cells against oxidative stress by inhibiting eNOS transcription and protein expression, but could not antagonise endotoxin induced cell injuries.