The Study Of Mechanism For GdCl3 Inducing Apoptosis Of AM On Severe Acute Pancreatitis In Rats

ObjectiveTo discuss the mechanism of gadolinium chloride inducing apoptosis of alveolarmacrophages of severe acute pancreatitis in rats by observing FasL expression inalveolar macrophages.Materials and MethodsExperimental SD rats were randomized into three groups(n=16 for each group):normal control group, severe acute pancreatitis group, gadolinium chloride treatmentgroup. Rat severe acute pancreatitis model was induced by intraductal administrationof 5% sodium taurocholate. Alveolar macrophages were obtained by bronchoalveolarlavage after six hours . Tumor necrosis factor-[alpha] and interleukin-1βof bronchoalveolar lavage fluids, the myeloperoxidase of lung tissue were evaluated. The lungtissue and pancreas tissue were examined by histology. The apoptosis of alveolarmacrophages was checked by transmission electric microscopy observation andAnnexin V/ propidium iodide double stained method. The expression of FasL inalveolar macrophages was analyzed by immunocytochemistry.ResultsThe apoptotic typical morphologic feature could be observed in alveolarmacrophages by transmission electric microscopy for gadolinium chloride treatmentgroups. Moreover, the indicators of myeloperoxidase and tumor necrosis factor-alphaand interleukin-1 betawere decreased and had statistical significance compared withsevere acute pancreatitis and normal control group (P<0.05). The rates of apoptosis ofalveolar macrophages had marked increase compared with normal control group andthe severe acute pancreatitis group (P<0.05). The cytochemistry showed there wasobvious expression of FasL in gadolinium chloride treatment group and had also thestatistical significance compared with the other groups (P<0.05).Conclusions Gadolinium chloride could induce apoptosis of alveolar macrophages throughactivating FasL pathway, then ameliorated lung injury associated with severe acutepancreatitis in rats.