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目的:探讨趋化因子fractalkine及其受体CX3CR1在大鼠肝肺综合征(HPS)发病机制中的作用。方法:将40只大鼠行胆总管结扎后随机均分为模型组与治疗组,5只大鼠仅游离胆总管不结扎,作为假手术组;治疗组大鼠于术后15~28 d腹腔内注射CX3CR1中和抗体,模型组组与假手术组大鼠给予等容量生理盐水代替。术后29 d检测大鼠肝功能、动脉血气,肺组织病理学、肺血管内巨噬细胞(PIM)、微血管密度(MVD)及CX3CR1的表达。结果:与假手术组比较,模型组大鼠血清谷丙转氨酶(ALT)、碱性磷酸酶(ALP)、总胆红素(TBIL)水平均明显升高,动脉血氧分压(PaO2)下降、肺泡-动脉血氧分压差(A-aDO2)升高,肺组织出现明显的病理改变、PIM(CD68表达量)、MVD增加(CD34表达量)、CX3CR1表达水平升高;治疗组大鼠肝功能也出现明显损伤,但好于模型组(均P<0.05),肺组织未见明显病理改变,血气指标、PIM、MVD、CX3CR1表达水平均无明显变化(均P>0.05)。结论:fractalkine/CX3CR1在肺组织中表达增加并结合是HPS肺组织巨噬细胞聚积及微血管增生的关键信号通路,阻断该信号通路可抑制HPS的发生与发展。
Objective: To investigate the role of fractalkine and its receptor CX3CR1 in the pathogenesis of hepatopulmonary syndrome (HPS) in rats. Methods: Forty rats were randomly divided into model group and treatment group after common bile duct ligation, and only 5 rats were not ligated with common bile duct. They were used as sham operation group. The rats in treatment group were sacrificed at 15-28 days after operation CX3CR1 neutralizing antibody was injected intraperitoneally, and the rats in model group and sham operation group were given the same volume of normal saline instead. On the 29th day after operation, the liver function, arterial blood gas, histopathology, pulmonary macrophage (PIM), microvessel density (MVD) and the expression of CX3CR1 were detected. Results: Compared with the sham operation group, the levels of serum ALT, ALP and TBIL in the model group were significantly increased, while the PaO2 decreased , The alveolar-arterial oxygen pressure difference (A-aDO2) increased, the pathological changes of lung tissue were observed. The expression of CD68 and MVD increased and the expression of CX3CR1 increased. (P <0.05). There was no obvious pathological changes in lung tissue. There was no significant change in the expression of blood gas, PIM, MVD and CX3CR1 (all P> 0.05). CONCLUSION: The increased expression of fractalkine / CX3CR1 in lung tissue is the key signal pathway of macrophage accumulation and microvascular hyperplasia in HPS lung. Blocking the signal pathway can inhibit the occurrence and development of HPS.