氯化钆抑制枯否细胞对大鼠肝脏缺血再灌注损伤的影响

Effect of inhibition of Kuppfer cells by gadolinium chloride on ischemia reperfusion injury in rat liver

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 inhibiting Kuppfer cells on rat hepatic ischemia reperfusion injury. Methods Eighty partial hepatic ischemia reperfusion models were prepared and protocol rats were administered with gadolinium chloride, while the control rats with normal saline. Blood pressure, heart rate, AST, TNF-α and IL-1 levels were measured, and morphological changes of liver tissue were observed under a microscope in both groups before and 5 min, 1 h and 6 h after reperfusion. Results The levels of TNF-α and IL-1 at 6 h after reperfusion were （0. 475± 0. 069）μg/L and （0. 221 ± 0. 056）μg/L respectively, significantly lower than those in control group （0. 831 ± 0. 167）μg/L and （0. 335 ±0.127） μg/L respectively, P〈 0.05. The changes in blood pressure, heart rate and AST between two groups also had statistically significant difference （ P 〈 0.05）. Damages to the ultrastructure in protocol group were significantly alleviated as compared with control group. Conclusion Inhibiting activation of Kupffer cells may attenuate hepatic ischemia reperfusion injury, and Kupffer cells may play an importantrole in hepatic ischemia reperfusion injury.