梗阻性黄疸大鼠枯否细胞Fcγ受体表达及胆酸治疗的影响

Expression of Fcγ receptor of Kupffer cells and role of bile acid in rats with obstructive jaundice

目的：探讨枯否细胞在梗阻性黄疸中吞噬功能的机理。方法：通过大鼠梗阻性黄疸（梗黄）模型，观察肝脏枯否细胞（Ｋｕｐｆｅｒｃｅｌ，ＫＣ）表面Ｆｃγ受体（ＦｃｒｅｃｅｐｔｏｒｆｏｒＩｇＧ，ＦｃγＲ）表达及胆酸治疗的影响。结果：梗黄时ＫＣＦｃγＲ表达减少（Ｐ＜０．０１）。ＫＣ吞噬功能下降，血内毒素浓度升高，且随着梗阻时间延长，三者分别呈进行性减少、下降及升高。胆酸治疗后ＫＣＦｃγＲ表达显著增加（Ｐ＜０．０１），ＫＣ吞噬功能呈同步变化，二者与内毒素浓度呈显著负相关。结论：梗黄时ＫＣ吞噬功能下降与ＫＣ表面ＦｃγＲ表达减少有关。胆酸治疗能有效降低血内毒素水平，增加ＫＣＦｃγＲ表达及ＫＣ吞噬功能。

Objective: To explore the mechanism of the inhibition of the phagocytic function of Kupffer cells (KCs) during obstructive jaundice(OJ). Methods: After the model of OJ was established in rats, the expression of Fcγ receptor (FcγR) of cultured KCs and the effects of bile acid on it were observed with cylometry. Meanwhile, the phagocytic function of KCs and the concentration of endotoxin in the plasma were also determined. Results: During OJ, the expression of FcγR and phagocytic function were significantly increased and they were significantly correlated with the concentration of endotoxin in the plasma. Conclusion: During OJ, the decrease of phagocytic function of KCs might be due to the decrease of the expression of FcγR and the treatment with bile acid can effectively decrease the concentration of endotoxin in plasma and hence the expression of FcγR and phagocytic function of KCs are enhanced.