| The structures and functions of human organs degenerate obviously in the process of aging and the function reserve of the most senile organs decreases. The senile people is susceptible to suffer the multiple organ dysfunction syndrome in the elderly (MODSE) by lung infections or injuries. But the mechanism of MODSE induced by pulmonary challenge in the elderly has not been interpreted clearly. Proteins, the basic substances sustaining for the life phenomena, can translate gene sequences into function. Investigating to changes of proteins in quantity and structures might be helpful to understand the mechanism of MODSE and decide the relative managements. Objective: To investigate the changes of lung proteins in elder rats with acute lung injury (ALI) induced by intratracheal LPS infusion and find clues on how lung triggers MODSE.Methods: Twelve SD rats were randomly assigned to two groups. One group was induced the acute lung injury by intratracheal administration of low dose lipopolysaccharide and the other was infused by sterile saline. The differences of the two groups in lung functions and pathologic structures were observed. The lung protein extracts from the two groups were analyzed by 2-DE and MAIDI-TOF-MS.Results: (1)Twelve hours after ALI induced LPS, arterial gas analysis showed respiratory function failure type II and respiratory acidosis. PaO2 and SaO2 of the subject reduced significantly (p<0.05) . (2) Lung index of the subjectincreased(0.54 ±0.04 vs. 0.42 ± 0.02, P<0.01). (3) The lungs of the rats with LPS showed pulmonary alveolar congestion, edema, exudation, capillary dilation and inflammatory cell infiltration in lung tissue. (4) The gels of the control by 2-DE had 730 ±52 spots and the gels of subject had 706±67spots with 86% of match rate. (5 ) By contrasting the gels, the sixteen different spots were found. The thirteen ones of them increased and the other three spots decreased. (6 ) These spots were analyzed by MALDI-TOF-MS and searched in the protein databank. Eight proteins were identified: heat shock 27kDa protein; peroxiredoxin; rnalate dehydrogenase; glutathione S-transferase; calpactin I heavy chain; carbonic anhydrase 2; Rho GDP dissociation inhibitor (GDI) alpha; endoplasmic retuclum protein 29.Conclusions: (1) Intratracheal administration of low dose lipopolysaccharide can induce ALI in senile rats; (2) The manifestation of ALI induced by LPS are pulmonary alveolar congestion, edema, exudation, capillary dilation and inflammatory cell infiltration in lung tissue; (3 ) ALI induced by LPS influence the oxygen exchanges between the capillaries and alveoli; (4) ALI induced by LPS can lead to the changes of the lung proteins: (5) 2-DE can separate these abnormal proteins from the others; (6) These abnormal proteins are mainly related with stresses, inflammatory reaction, energy and lipids metabolism, detoxifcation, oxidants and free radicals elimination.
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