2002•Zhongguo dangdai erke zazhiRequires access

Hepatic Injuries Induced by Endotoxin and the Protective Effect of Dexamethasone on the Liver of Neonatal Rats

Yu Wu

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Abstract

Objective To observe the dynamic changes of nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) and the protective effect of dexamethasone (Dex) on the liver when Lipopolysaccharide (LPS) induces hepatic injuries in neonatal rats. Methods One hundred and twenty seven day neonatal rats were divided into the control group (Group A), LPS group (Group B), and Dex group (Group C). Group B rats received 5 mg/kg LPS intraparitoneally. Group C was given LPS 5 mg/kg+Dex 5 mg/kg, and Group A was injected with normal saline of the same volume. NO and MDA contents and SOD activity were detected by the biochemical method in the liver tissues at different times. At the same time, the structural changes of the liver were observed under the light microscope and electron microscope. Results ① NO and MDA contents increased in Group B compared with Group A. NO content reached its maximum [( 2.58 ± 0.31 ) μmol/g.pro] at 6 h after LPS was given (P 0.01 ); MDA content reached its maximum [( 2.61 ± 0.50 ) nmol/mg.pro] at 4 h after LPS was given (P 0.05 ). SOD activity in Group B decreased as time was increasing compared with Group A. It dropped to its minimum [( 118.96 ± 12.81 ) NU/mg.pro] at 24 h (P 0.01 ). NO and MDA contents decreased significantly and SOD activity increased significantly at 4 h and 6 h in Group C compared with Group B (P 0.05 or 0.01 ). ② In group B, a large amount of inflammatory cell infiltration in liver tissues were noted and hepatic cells showed spotty necrosis and bleeding under the light microscope; the electron microscope showed a significant decrease of mitochondria cristae, the broadness of endoplasmic reticula, hepatic cell necrosis and karyopyknosis. The structural changes were alleviated in Group C. Conclusions LPS could cause changes of NO and MDA contents and SOD activity in hepatic tissues. Dex might inhibit NO production and get rid of oxygen free radicals so that it can protect the liver from injuries.

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Objective To observe the dynamic changes of nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) and the protective effect of dexamethasone (Dex) on the liver when Lipopolysaccharide (LPS) induces hepatic injuries in neonatal rats. Methods One hundred and twenty seven day neonatal rats were divided into the control group (Group A), LPS group (Group B), and Dex group (Group C). Group B rats received 5 mg/kg LPS intraparitoneally. Group C was given LPS 5 mg/kg+Dex 5 mg/kg, and Group A was injected with normal saline of the same volume. NO and MDA contents and SOD activity were detected by the biochemical method in the liver tissues at different times. At the same time, the structural changes of the liver were observed under the light microscope and electron microscope. Results ① NO and MDA contents increased in Group B compared with Group A. NO content reached its maximum [( 2.58 ± 0.31 ) μmol/g.pro] at 6 h after LPS was given (P 0.01 ); MDA content reached its maximum [( 2.61 ± 0.50 ) nmol/mg.pro] at 4 h after LPS was given (P 0.05 ). SOD activity in Group B decreased as time was increasing compared with Group A. It dropped to its minimum [( 118.96 ± 12.81 ) NU/mg.pro] at 24 h (P 0.01 ). NO and MDA contents decreased significantly and SOD activity increased significantly at 4 h and 6 h in Group C compared with Group B (P 0.05 or 0.01 ). ② In group B, a large amount of inflammatory cell infiltration in liver tissues were noted and hepatic cells showed spotty necrosis and bleeding under the light microscope; the electron microscope showed a significant decrease of mitochondria cristae, the broadness of endoplasmic reticula, hepatic cell necrosis and karyopyknosis. The structural changes were alleviated in Group C. Conclusions LPS could cause changes of NO and MDA contents and SOD activity in hepatic tissues. Dex might inhibit NO production and get rid of oxygen free radicals so that it can protect the liver from injuries.

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Available abstract

Objective To observe the dynamic changes of nitric oxide (NO), superoxide dismutase (SOD) and malondialdehyde (MDA) and the protective effect of dexamethasone (Dex) on the liver when Lipopolysaccharide (LPS) induces hepatic injuries in neonatal rats. Methods One hundred and twenty seven day neonatal rats were divided into the control group (Group A), LPS group (Group B), and Dex group (Group C). Group B rats received 5 mg/kg LPS intraparitoneally. Group C was given LPS 5 mg/kg+Dex 5 mg/kg, and Group A was injected with normal saline of the same volume. NO and MDA contents and SOD activity were detected by the biochemical method in the liver tissues at different times. At the same time, the structural changes of the liver were observed under the light microscope and electron microscope. Results ① NO and MDA contents increased in Group B compared with Group A. NO content reached its maximum [( 2.58 ± 0.31 ) μmol/g.pro] at 6 h after LPS was given (P 0.01 ); MDA content reached its maximum [( 2.61 ± 0.50 ) nmol/mg.pro] at 4 h after LPS was given (P 0.05 ). SOD activity in Group B decreased as time was increasing compared with Group A. It dropped to its minimum [( 118.96 ± 12.81 ) NU/mg.pro] at 24 h (P 0.01 ). NO and MDA contents decreased significantly and SOD activity increased significantly at 4 h and 6 h in Group C compared with Group B (P 0.05 or 0.01 ). ② In group B, a large amount of inflammatory cell infiltration in liver tissues were noted and hepatic cells showed spotty necrosis and bleeding under the light microscope; the electron microscope showed a significant decrease of mitochondria cristae, the broadness of endoplasmic reticula, hepatic cell necrosis and karyopyknosis. The structural changes were alleviated in Group C. Conclusions LPS could cause changes of NO and MDA contents and SOD activity in hepatic tissues. Dex might inhibit NO production and get rid of oxygen free radicals so that it can protect the liver from injuries.

Key concepts: Malondialdehyde, Superoxide dismutase, Lipopolysaccharide, Dexamethasone, Endocrinology, Internal medicine, Nitric oxide, Group B

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