2017•Zhonghua mazuixue zazhiRequires access

Effect of propofol pretreatment on NF-κB activity during hepatic ischemia-reperfusion injury in rats

Ge Zhao, Ruijing Huang, Na Duan, Xin Shen, Qiang Wang

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Abstract

Objective To evaluate the effect of propofol pretreatment on nuclear factor kappa B (NF-κB) activity during hepatic ischemia-reperfusion (I/R) injury in rats. Methods Twenty-four pathogen-free healthy male Sprague-Dawley rats, aged 2 months, weighing 200-250 g, were divided into 3 groups (n=8 each) using a random number table: sham operation group (group S), group I/R and propofol pretreatment group (group P). Hepatic I/R injury was induced by 45 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by reperfusion. In group P, propofol 12 mg·kg-1·h-1 was infused via the femoral vein until the end of ischemia starting from 30 min before ischemia in group P. Blood samples were collected from the inferior vena cava at 120 min of reperfusion for determination of the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The rats were then sacrificed and livers were removed for determination of phosphorylated NF-κB p65 (p-NF-κB p65) expression in liver tissues (by Western blot) and apoptosis in hepatocytes (by TUNEL). Apoptosis index (AI) was calculated. Results Compared with group S, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly increased, and the expression of p-NF-κB p65 in liver tissues was up-regulated in I/R and P groups (P<0.05). Compared with group I/R, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly decreased, and the expression of p-NF-κB p65 in liver tissues was down-regulated in group P (P<0.05). Conclusion The mechanism by which propofol pretreatment reduces hepatic I/R injury is associated with inhibiting NF-κB activity in rats. Key words: Propofol; Liver; Reperfusion injury

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Objective To evaluate the effect of propofol pretreatment on nuclear factor kappa B (NF-κB) activity during hepatic ischemia-reperfusion (I/R) injury in rats. Methods Twenty-four pathogen-free healthy male Sprague-Dawley rats, aged 2 months, weighing 200-250 g, were divided into 3 groups (n=8 each) using a random number table: sham operation group (group S), group I/R and propofol pretreatment group (group P). Hepatic I/R injury was induced by 45 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by reperfusion. In group P, propofol 12 mg·kg-1·h-1 was infused via the femoral vein until the end of ischemia starting from 30 min before ischemia in group P. Blood samples were collected from the inferior vena cava at 120 min of reperfusion for determination of the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The rats were then sacrificed and livers were removed for determination of phosphorylated NF-κB p65 (p-NF-κB p65) expression in liver tissues (by Western blot) and apoptosis in hepatocytes (by TUNEL). Apoptosis index (AI) was calculated. Results Compared with group S, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly increased, and the expression of p-NF-κB p65 in liver tissues was up-regulated in I/R and P groups (P<0.05). Compared with group I/R, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly decreased, and the expression of p-NF-κB p65 in liver tissues was down-regulated in group P (P<0.05). Conclusion The mechanism by which propofol pretreatment reduces hepatic I/R injury is associated with inhibiting NF-κB activity in rats. Key words: Propofol; Liver; Reperfusion injury

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Available abstract

Objective To evaluate the effect of propofol pretreatment on nuclear factor kappa B (NF-κB) activity during hepatic ischemia-reperfusion (I/R) injury in rats. Methods Twenty-four pathogen-free healthy male Sprague-Dawley rats, aged 2 months, weighing 200-250 g, were divided into 3 groups (n=8 each) using a random number table: sham operation group (group S), group I/R and propofol pretreatment group (group P). Hepatic I/R injury was induced by 45 min occlusion of the hepatic artery and portal vein entering the middle and left lobes of the liver followed by reperfusion. In group P, propofol 12 mg·kg-1·h-1 was infused via the femoral vein until the end of ischemia starting from 30 min before ischemia in group P. Blood samples were collected from the inferior vena cava at 120 min of reperfusion for determination of the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β). The rats were then sacrificed and livers were removed for determination of phosphorylated NF-κB p65 (p-NF-κB p65) expression in liver tissues (by Western blot) and apoptosis in hepatocytes (by TUNEL). Apoptosis index (AI) was calculated. Results Compared with group S, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly increased, and the expression of p-NF-κB p65 in liver tissues was up-regulated in I/R and P groups (P<0.05). Compared with group I/R, the levels of ALT, AST, TNF-α and IL-1β in serum and AI were significantly decreased, and the expression of p-NF-κB p65 in liver tissues was down-regulated in group P (P<0.05). Conclusion The mechanism by which propofol pretreatment reduces hepatic I/R injury is associated with inhibiting NF-κB activity in rats. Key words: Propofol; Liver; Reperfusion injury

Key concepts: Propofol, Medicine, Reperfusion injury, Ischemia, TUNEL assay, Apoptosis, Endocrinology, Inferior vena cava

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Effect of propofol pretreatment on NF-κB activity during hepatic ischemia-reperfusion injury in rats — Research Paper | ScholarLens