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目的探讨抑制枯否细胞对大鼠肝脏缺血再灌注损伤的影响。方法制作部分肝脏缺血再灌注大鼠模型80只,实验组注射氯化钆,对照组注射生理盐水,检测两组大鼠缺血前、再灌注后5min、1和6h血压、心率的变化,血清转氨酶(AST)、肿瘤坏死因子α(TNFα)和白细胞介素1(IL1)的水平及肝组织超微结构的改变。结果实验组再灌注6h血清TNFα和IL1为(0.475±0.069)μg/L和(0.221±0.056)μg/L,显著低于对照组的(0.831±0.167)μg/L和(0.335±0.127)μg/L(P<0.05),两组血压、心率和AST变化的差异也有统计学意义(P<0.05),实验组大鼠肝脏超微结构的损伤程度轻于对照组。结论抑制枯否细胞活化可减轻肝脏缺血再灌注损伤,枯否细胞在肝脏缺血再灌注损伤中的作用很重要。
Objective To investigate the effects of inhibition of Kupffer cells on hepatic ischemia-reperfusion injury in rats. Methods Totally 80 rats with partial hepatic ischemia-reperfusion injury were injected with GdCl4 in experimental group and normal saline in control group. The changes of blood pressure and heart rate were measured before ischemia, 5min, 1h and 6h after reperfusion. The levels of serum aminotransferase (AST), tumor necrosis factor alpha (TNFα) and interleukin 1 (IL1) and the ultrastructure of hepatic tissue were detected. Results The levels of TNFα and IL1 in the experimental group at 6h after reperfusion were (0.475 ± 0.069) μg / L and (0.221 ± 0.056) μg / L, respectively, which were significantly lower than those in the control group (0.831 ± 0.167) and 0.335 ± 0.127 /L (P <0.05). There was also a significant difference in blood pressure, heart rate and AST between the two groups (P <0.05). The degree of liver ultrastructure damage in the experimental group was lighter than that in the control group. Conclusion Inhibition of Kupffer cell activation can reduce hepatic ischemia-reperfusion injury and the role of Kupffer cells in liver ischemia-reperfusion injury is very important.