Abstract:Objective To discuss the mechanism of apoptosis of alveolar macrophages(AM) in severe acute pancreatitis (SAP)induced by gadolinium chloride(GdCl3).
Methods Forty-eight SD rats were randomized into three groups(n=16 for each group): normal control group, SAP group, and GdCl3treatment group. Rat SAP model was induced by retrograde intraductal administration of 5% sodium taurocholate. Alveolar macrophages(AM) were obtained by bronchoalveolar lavage. Tumor necrosis factor-alpha (TNF-α) and interleukin 1β（IL-1β）of bronchoalveolar lavage fluids (BALF) were evaluated. The lung tissue and pancreas tissue were examined by histology.The apoptosis of AM was checked by transmission electric microscopy and cytometry Annexin V/FITC and propidium iodide (PI) double stained method. The expression of FasL in AM was analyzed by immunohistochemistry.
Results Transmission electric microscopy showed the typical apoptotic morphologic feature of AM in GdCl3 treatment group. The levels of TNFα and IL-1β in GdCl3 treatment group were (7.84±0.75)pg/mL，(8.57±5.64)pg/mL respectively, were significanty less than SAP group (P<0.05). Moreover, the rates of apoptosis of AM and expression of FasL in GdCl3 treatment group［(22.48±1.44)%, (41.67±11.69)% respectively］were obviously increased compared with the other two groups (P<0.05). The apoptosis rate of AM had positive correlation with the positive expression of FasL（r＝0.835，P<0.001）.
Conclusions GdCl3 could induce the apoptosis of AM by activating expression of FasL, and then can ameliorate the lung injury associated with SAP.