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Expression changes of TNF-α, IL-1β and IL-6 in the rat lung of decompression sickness induced by fast buoyancy ascent escape.
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2015
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Acute Lung InjuryInflammatory Lung DiseaseLung InflammationExpression ChangesImmunologyImmune RegulationInnate ImmunityRat ModelRat LungInflammationDisease PathophysiologyPulmonary PharmacologyPulmonary CirculationChronic InflammationImmune FunctionInflammatory DiseaseCytokinePhysiologyPulmonary PhysiologyLung MechanicsDecompression SicknessMedicine
Fast buoyancy ascent escape is the general submarine escape manner adopted by the majority of naval forces all over the world. However, if hyperbaric exposure time exceeds the time limit, fast buoyancy ascent escape has a high risk to result in decompression sickness (DCS). Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and IL-6 have been all implicated in the process of inflammation associated with acute lung injury (ALI). Our work demonstrated that DCS caused by simulated fast buoyancy ascent escape could induce ALβ in the rat model. The purpose of the present work was to study the expression changes of TNF-α, IL-1β and IL-6 in the rat lung affected by DCS caused by simulated fast buoyancy ascent escape. The lung tissue mRNA levels of TNF-α, Il-1β and Il-6 were significantly increased at 0.5 hour after DCS caused by simulated fast buoyancy ascent escape. The lung contents of TNF-α, IL-1β and IL-6 were at an expression peak at 0.5 hour, although showing no statistical difference when compared with the normal control group. In conclusion, the rat lung expression variations of TNF-α, IL-1β and IL-6 are the most obvious at 0.5 hour within 24 hours after the lung injury by DCS caused by simulated fast buoyancy ascent escape.