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目的观察大鼠在肝脏缺血再灌注(IR)过程中肝脏炎性细胞因子TNFα、IL1βmRNA表达与脑组织NFκB、ICAM1表达之间的关系,探讨肝脏IR是否可导致脑组织损伤及其可能的机制。方法选健康雄性Wister大鼠48只,随机分为对照组、缺血30min组(I组)、缺血30min再灌注组(IR组)、缺血30min再灌注后1h组(IR1h组)、缺血30min再灌注后2h组(IR2h组)、缺血30min再灌注后4h组(IR4h组),每组8只。应用免疫组化法分别检测各组大鼠肝脏TNFα及脑皮质、海马和下丘脑区NFκB、ICAM1的表达情况,应用原位杂交的方法检测肝脏IL1βmRNA表达情况。结果肝脏IR导致肝脏明显的损伤,表现为血清GPT、AKP、γGT升高(P<0.01),肝组织中TNFα、IL1βmRNA表达显著增加(P<0.01),肝细胞水肿,炎性细胞浸润,甚至细胞坏死。随着再灌注时间的延长,脑组织HE染色可见脑细胞水肿,甚至个别脑细胞坏死。与对照组比较,I组和IR组大鼠脑皮质、海马和下丘脑中NFκB、ICAM1表达的差异无统计学意义(P>0.05),IR1h组、IR2h组和IR4h组的差异有统计学意义(P<0.05,P<0.01)。IR1h、IR2h、IR4h组与对照组、I组、IR组比较,各部位脑组织NFκB、ICAM1的表达显著增加(P<0.05或P<0.01)。各组大鼠不同部位脑组织间NFκB、ICAM1表达无统计学意义(P>0.05)。结论肝脏IR对脑组织可产?
Objective To observe the relationship between the expression of inflammatory cytokines TNFα and IL1βmRNA and the expression of NFκB and ICAM1 during the process of hepatic ischemia-reperfusion (I / R) in rats, and to explore whether hepatic IR can cause brain injury and its possible mechanism . Methods Forty-eight healthy male Wister rats were randomly divided into control group, ischemia group 30min (group I), ischemia 30min group IR (IR), ischemia 30h and group IR1h After 30min reperfusion, blood was collected for 2 hours (IR2h group), ischemia-reperfusion 30min ischemia group (IR4h group), 8 rats in each group. Immunohistochemistry was used to detect the expression of TNFα, NFκB and ICAM1 in the cortex, hippocampus and hypothalamus in the liver of rats in each group. The expression of IL1βmRNA in the liver was detected by in situ hybridization. Results The hepatic IR caused significant hepatic injury. The serum levels of GPT, AKP and γGT were significantly increased (P <0.01), and the expressions of TNFα and IL1β mRNA were significantly increased (P <0.01). Hepatic edema, inflammatory cell infiltration and even Cell necrosis. With the reperfusion time, brain tissue HE staining brain cell edema, and even individual brain cell necrosis. Compared with the control group, there was no significant difference in NFκB and ICAM1 expression in cerebral cortex, hippocampus and hypothalamus between I and IR groups (P> 0.05), and there was significant difference between IR1h group, IR2h group and IR4h group (P <0.05, P <0.01). The expressions of NFκB and ICAM1 were significantly increased in IR1h, IR2h and IR4h groups compared with the control group, I group and IR group (P <0.05 or P <0.01). There was no significant difference in the expression of NFκB and ICAM1 between different groups of rats in each group (P> 0.05). Conclusion Liver IR can produce brain tissue?