2014•Zhonghua mazuixue zazhiRequires access

Effect of ulinastatin on brain injury induced by lipopolysaccharide in mice

Wenyao Li, Guocai Tao

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Abstract

Objective To evaluate the effect of ulinastatin on brain injury induced by lipopolysaccharide (LPS) in mice.Methods Ninety adult male C57 mice,aged 3-4 months,weighing 200-300 g,were randomly divided into 3 groups (n =30 each) using a random number table:control group (C group),LPS group and ulinastatin group (U group).Group U received intraperitoneal injection of ulinastatin 10 000 U/kg,while group L received the equal volume of normal saline,and 10 min later brain injury was produced with LPS 1 μg/g injected into the cerebral ventricle.Ten animals were chosen and blood samples were taken for determination of plasma concentrations of S100β protein and neuron-specific enolase (NSE) at 1,3 and 7 days after LPS injection.Then the animals were sacrificed and hippocampal tissues were obtained for determination of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α) contents and IL-1β mRNA and TNF-α mRNA expression.Results Compared with C group,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased at 1,3 and 7 days after LPS injection,and IL-1β mRNA and TNF-α mRNA expression was up-regulated at 1 and 3 days after LPS injection in LPS and U groups.Compared with group LPS,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased,and IL-1β mRNA and TNF-α mRNA expression was down-regulated at 1 and 3 days after LPS injection in group U.Conclusion Ulinastatin can attenuate brain injury induced by LPS in mice,and the mechanism is related to inhibited inflammatory responses. Key words: Trypsin inhibitors ;  Endotoxemia;  Brain injuries

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Objective To evaluate the effect of ulinastatin on brain injury induced by lipopolysaccharide (LPS) in mice.Methods Ninety adult male C57 mice,aged 3-4 months,weighing 200-300 g,were randomly divided into 3 groups (n =30 each) using a random number table:control group (C group),LPS group and ulinastatin group (U group).Group U received intraperitoneal injection of ulinastatin 10 000 U/kg,while group L received the equal volume of normal saline,and 10 min later brain injury was produced with LPS 1 μg/g injected into the cerebral ventricle.Ten animals were chosen and blood samples were taken for determination of plasma concentrations of S100β protein and neuron-specific enolase (NSE) at 1,3 and 7 days after LPS injection.Then the animals were sacrificed and hippocampal tissues were obtained for determination of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α) contents and IL-1β mRNA and TNF-α mRNA expression.Results Compared with C group,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased at 1,3 and 7 days after LPS injection,and IL-1β mRNA and TNF-α mRNA expression was up-regulated at 1 and 3 days after LPS injection in LPS and U groups.Compared with group LPS,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased,and IL-1β mRNA and TNF-α mRNA expression was down-regulated at 1 and 3 days after LPS injection in group U.Conclusion Ulinastatin can attenuate brain injury induced by LPS in mice,and the mechanism is related to inhibited inflammatory responses. Key words: Trypsin inhibitors ;  Endotoxemia;  Brain injuries

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Available abstract

Objective To evaluate the effect of ulinastatin on brain injury induced by lipopolysaccharide (LPS) in mice.Methods Ninety adult male C57 mice,aged 3-4 months,weighing 200-300 g,were randomly divided into 3 groups (n =30 each) using a random number table:control group (C group),LPS group and ulinastatin group (U group).Group U received intraperitoneal injection of ulinastatin 10 000 U/kg,while group L received the equal volume of normal saline,and 10 min later brain injury was produced with LPS 1 μg/g injected into the cerebral ventricle.Ten animals were chosen and blood samples were taken for determination of plasma concentrations of S100β protein and neuron-specific enolase (NSE) at 1,3 and 7 days after LPS injection.Then the animals were sacrificed and hippocampal tissues were obtained for determination of interleukin-1β (IL-1 β) and tumor necrosis factor-α (TNF-α) contents and IL-1β mRNA and TNF-α mRNA expression.Results Compared with C group,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased at 1,3 and 7 days after LPS injection,and IL-1β mRNA and TNF-α mRNA expression was up-regulated at 1 and 3 days after LPS injection in LPS and U groups.Compared with group LPS,the plasma concentrations of S100β protein and NSE and contents of IL-1β and TNF-α were significantly increased,and IL-1β mRNA and TNF-α mRNA expression was down-regulated at 1 and 3 days after LPS injection in group U.Conclusion Ulinastatin can attenuate brain injury induced by LPS in mice,and the mechanism is related to inhibited inflammatory responses. Key words: Trypsin inhibitors ;  Endotoxemia;  Brain injuries

Key concepts: Ulinastatin, Lipopolysaccharide, Enolase, Tumor necrosis factor alpha, Endocrinology, Saline, Intraperitoneal injection, Internal medicine

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