Objective:To study the effect of inhibiting P38 mitogen activated protein kinase (P38MAPK) on inflammatory factors and cell apoptosis during flap ischemia-reperfusion injury. Methods:Wistar rats were selected as exper...Objective:To study the effect of inhibiting P38 mitogen activated protein kinase (P38MAPK) on inflammatory factors and cell apoptosis during flap ischemia-reperfusion injury. Methods:Wistar rats were selected as experimental animals and randomly divided into control group, model group and intervention group (n=12), control group were made into routine abdominal superficial arteriovenous flap models, model group were made into ischemia-reperfusion flap models and intervention group were made into ischemia-reperfusion flap models and then received SB202190 intervention. 8 d after flap making, tissue was collected to detect the expression of inflammatory factors and apoptosis molecules as well as the levels of oxidative stress indicators.Results:NF-κB, IL-6, TNF-α, Bax and Caspase-3 mRNA expression and protein expression in flap tissue of model group were significantly higher than those of control group (P<0.05), ROS, MDA, AOPP and 8-OHdG levels were significantly higher than those of control group, and Bcl-2 mRNA expression and protein expression were significantly lower than those of control group (P<0.05);NF-κB, IL-6, TNF-α, Bax and Caspase-3 mRNA expression and protein expression in flap tissue of intervention group were significantly lower than those of model group (P<0.05), ROS, MDA, AOPP and 8-OHdG levels were significantly lower than those of model group (P<0.05), and Bcl-2 mRNA expression and protein expression were significantly higher than those of model group (P<0.05).Conclusions:Inhibiting P38MAPK can reduce the transplanted flap ischemia-reperfusion injury caused by inflammation, oxidative stress and cell apoptosis.展开更多
文摘Objective:To study the effect of inhibiting P38 mitogen activated protein kinase (P38MAPK) on inflammatory factors and cell apoptosis during flap ischemia-reperfusion injury. Methods:Wistar rats were selected as experimental animals and randomly divided into control group, model group and intervention group (n=12), control group were made into routine abdominal superficial arteriovenous flap models, model group were made into ischemia-reperfusion flap models and intervention group were made into ischemia-reperfusion flap models and then received SB202190 intervention. 8 d after flap making, tissue was collected to detect the expression of inflammatory factors and apoptosis molecules as well as the levels of oxidative stress indicators.Results:NF-κB, IL-6, TNF-α, Bax and Caspase-3 mRNA expression and protein expression in flap tissue of model group were significantly higher than those of control group (P<0.05), ROS, MDA, AOPP and 8-OHdG levels were significantly higher than those of control group, and Bcl-2 mRNA expression and protein expression were significantly lower than those of control group (P<0.05);NF-κB, IL-6, TNF-α, Bax and Caspase-3 mRNA expression and protein expression in flap tissue of intervention group were significantly lower than those of model group (P<0.05), ROS, MDA, AOPP and 8-OHdG levels were significantly lower than those of model group (P<0.05), and Bcl-2 mRNA expression and protein expression were significantly higher than those of model group (P<0.05).Conclusions:Inhibiting P38MAPK can reduce the transplanted flap ischemia-reperfusion injury caused by inflammation, oxidative stress and cell apoptosis.
