2006Chinese Journal of Critical Care MedicineRequires access

Effects of propofol on the expression of aquaporin-1 in lipopolysaccharide-activated rat lung microvessel endothelial cells

Xiang Dong-mei

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Abstract

Objective To investigate the effects of propofol on the expression of aquaporin-1(AQP-l) of rat lung(microvessel) endothelial cells(RLMECs) induced by lipopolysaccharide(LPS).Methods Rat lung microvessel endothelial cells were randomly assigned to one of the following seven groups: no additives(negative control),LPS alone(0.1 μg/mL,1 μg/mL and 10 μg/mL),LPS(10 μg/mL) combination with either propofol(4 μg/mL or 40 μg/mL) or introlipid(40 μg/mL).Changes of osmotic reflection coefficients(σ) were measured,and expression of aquaporin-1(AQP-l) measured by immunocytochemistry and western blotting were also observed in cultured RLMECs.Results AQP-l protein expression and osmotic reflection coefficients(σ) values in LPS alone group,(specially) in high dose LPS alone group,were significantly lower than those in the normal control group(P0.01).The co-treatment of propofol and lipopolysaccharide significantly increased the protein expression of AQP-l and the osmotic reflection coefficients(σ) values(P0.01),while introlipid had no such benefical effects.Conclusions LPS stimulation can significantly decrease AQP-l expression.Propofol rather than intralipid,may take part in regulating AQP-l expression of RLMECs and attenuate LPS-induced abnormal fluid transportation in acute lung injury.

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Objective To investigate the effects of propofol on the expression of aquaporin-1(AQP-l) of rat lung(microvessel) endothelial cells(RLMECs) induced by lipopolysaccharide(LPS).Methods Rat lung microvessel endothelial cells were randomly assigned to one of the following seven groups: no additives(negative control),LPS alone(0.1 μg/mL,1 μg/mL and 10 μg/mL),LPS(10 μg/mL) combination with either propofol(4 μg/mL or 40 μg/mL) or introlipid(40 μg/mL).Changes of osmotic reflection coefficients(σ) were measured,and expression of aquaporin-1(AQP-l) measured by immunocytochemistry and western blotting were also observed in cultured RLMECs.Results AQP-l protein expression and osmotic reflection coefficients(σ) values in LPS alone group,(specially) in high dose LPS alone group,were significantly lower than those in the normal control group(P0.01).The co-treatment of propofol and lipopolysaccharide significantly increased the protein expression of AQP-l and the osmotic reflection coefficients(σ) values(P0.01),while introlipid had no such benefical effects.Conclusions LPS stimulation can significantly decrease AQP-l expression.Propofol rather than intralipid,may take part in regulating AQP-l expression of RLMECs and attenuate LPS-induced abnormal fluid transportation in acute lung injury.

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Available abstract

Objective To investigate the effects of propofol on the expression of aquaporin-1(AQP-l) of rat lung(microvessel) endothelial cells(RLMECs) induced by lipopolysaccharide(LPS).Methods Rat lung microvessel endothelial cells were randomly assigned to one of the following seven groups: no additives(negative control),LPS alone(0.1 μg/mL,1 μg/mL and 10 μg/mL),LPS(10 μg/mL) combination with either propofol(4 μg/mL or 40 μg/mL) or introlipid(40 μg/mL).Changes of osmotic reflection coefficients(σ) were measured,and expression of aquaporin-1(AQP-l) measured by immunocytochemistry and western blotting were also observed in cultured RLMECs.Results AQP-l protein expression and osmotic reflection coefficients(σ) values in LPS alone group,(specially) in high dose LPS alone group,were significantly lower than those in the normal control group(P0.01).The co-treatment of propofol and lipopolysaccharide significantly increased the protein expression of AQP-l and the osmotic reflection coefficients(σ) values(P0.01),while introlipid had no such benefical effects.Conclusions LPS stimulation can significantly decrease AQP-l expression.Propofol rather than intralipid,may take part in regulating AQP-l expression of RLMECs and attenuate LPS-induced abnormal fluid transportation in acute lung injury.

Key concepts: Lipopolysaccharide, Microvessel, Propofol, Medicine, Aquaporin 1, Aquaporin, Endothelial stem cell, Aquaporin 4

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