2011Zhonghua mazuixue zazhiRequires access

Effects of propofol on lipopolysaccharide-induced brain injury in rats

Huiling Cao, Dan Ling, Wei Li

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Abstract

Objective To investigate the effects of propofol on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Fifty-four pathogen-free SD rats of both sexes, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups: control group (group C, n = 6) ; LPS group (group L, n = 24) ; propofol group (group P, n = 24) . Brain injury was produced by injection of LPS 1 mg/kg via the left internal carotid artery in L and P groups. Propofol 100 mg/kg was injected intraperitonealry immediately after the LPS administration in group P, while the equal volume of normal saline was given instead of propofol in group L. The equal volume of normal saline was given instead of LPS and propofol in group C. Six rats in each group were sacrificed and the brain tissues were immediately removed at 24 h after intraperitoneal administration in group C, and at 6, 24, 48 and 72 h after intraperitoneal administration in L and P groups for determination of brain water content, high-mobility group box 1 ( HMGB1) expression and NF-κB activity, and microscopic examination. Results The brain water content and NF-kB activity were significantly increased, and HMGB1 expression was up-regulated in group L as compared to group C (P < 0.05) . The brain water content, expression of HMGB1 and NF-kB activity were significantly lower in group P than in group L ( P < 0.05) . The microscopic examination showed that brain injury was attenuated in group P compared with group L. The brain water content was positively correlated with the HMGB1 expression and NF- κB activity (r = 0.692 and 0.769 respectively, P < 0.05). Conclusion Propofol can reduce the LPS- induced brain injury by reducing inflammatory response of the brain tissues. Key words: Propofol;  Brain injuries;  Endotoxemia

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Objective To investigate the effects of propofol on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Fifty-four pathogen-free SD rats of both sexes, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups: control group (group C, n = 6) ; LPS group (group L, n = 24) ; propofol group (group P, n = 24) . Brain injury was produced by injection of LPS 1 mg/kg via the left internal carotid artery in L and P groups. Propofol 100 mg/kg was injected intraperitonealry immediately after the LPS administration in group P, while the equal volume of normal saline was given instead of propofol in group L. The equal volume of normal saline was given instead of LPS and propofol in group C. Six rats in each group were sacrificed and the brain tissues were immediately removed at 24 h after intraperitoneal administration in group C, and at 6, 24, 48 and 72 h after intraperitoneal administration in L and P groups for determination of brain water content, high-mobility group box 1 ( HMGB1) expression and NF-κB activity, and microscopic examination. Results The brain water content and NF-kB activity were significantly increased, and HMGB1 expression was up-regulated in group L as compared to group C (P < 0.05) . The brain water content, expression of HMGB1 and NF-kB activity were significantly lower in group P than in group L ( P < 0.05) . The microscopic examination showed that brain injury was attenuated in group P compared with group L. The brain water content was positively correlated with the HMGB1 expression and NF- κB activity (r = 0.692 and 0.769 respectively, P < 0.05). Conclusion Propofol can reduce the LPS- induced brain injury by reducing inflammatory response of the brain tissues. Key words: Propofol;  Brain injuries;  Endotoxemia

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Available abstract

Objective To investigate the effects of propofol on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Fifty-four pathogen-free SD rats of both sexes, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups: control group (group C, n = 6) ; LPS group (group L, n = 24) ; propofol group (group P, n = 24) . Brain injury was produced by injection of LPS 1 mg/kg via the left internal carotid artery in L and P groups. Propofol 100 mg/kg was injected intraperitonealry immediately after the LPS administration in group P, while the equal volume of normal saline was given instead of propofol in group L. The equal volume of normal saline was given instead of LPS and propofol in group C. Six rats in each group were sacrificed and the brain tissues were immediately removed at 24 h after intraperitoneal administration in group C, and at 6, 24, 48 and 72 h after intraperitoneal administration in L and P groups for determination of brain water content, high-mobility group box 1 ( HMGB1) expression and NF-κB activity, and microscopic examination. Results The brain water content and NF-kB activity were significantly increased, and HMGB1 expression was up-regulated in group L as compared to group C (P < 0.05) . The brain water content, expression of HMGB1 and NF-kB activity were significantly lower in group P than in group L ( P < 0.05) . The microscopic examination showed that brain injury was attenuated in group P compared with group L. The brain water content was positively correlated with the HMGB1 expression and NF- κB activity (r = 0.692 and 0.769 respectively, P < 0.05). Conclusion Propofol can reduce the LPS- induced brain injury by reducing inflammatory response of the brain tissues. Key words: Propofol;  Brain injuries;  Endotoxemia

Key concepts: Propofol, Saline, Lipopolysaccharide, Intraperitoneal injection, Anesthesia, HMGB1, Medicine, Endocrinology

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