ENGLISH ABSTRACT
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
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[Activation of p38 mitogen-activated protein kinase pathway in ventilator-induced lung injury in rat].

OBJECTIVE: To study the activation of p38 mitogen-activated protein kinase (MAPK) and the expression of inflammatory cytokines in ventilator-induced lung injury (VILI) in rat.

METHODS: Thirty healthy male SD rats were randomly divided into three group (A, B, C group, n=10 per group). Mechanical ventilation was instituted in all the groups. A group: tidal volume (V(T))=8 ml/kg, respiratory rate (RR)=80/min; B group: V(T)=20 ml/kg, RR=80/min; C group: V(T)=40 ml/kg, RR=80/min. The time of ventilation for all the groups was two hours. Rats were sacrificed after experiment was finished. The bronchial lavage liquid and lung tissue were collected and stored with routine methods. The pathological changes in lung tissue were examined with optical microscope. The expression of p38 and phos-p38 (p-p38) were measured by Western blotting in lung tissues. The expression of intercellular adhesion molecular-1 (ICAM-1) was detected by reverse transcriptase-polymerase chain reaction (RT-PCR). The contents of total protein, white blood cells (WBC), myeloperoxidase (MPO), macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-alpha (TNF-alpha) were also determined.

RESULTS: Compared with A group, total protein, WBC, MPO, MIP-2, TNF-alpha, ICAM-1 and p-p38 were significantly increased in B group and C group (all P<0.01). Compared with B group, the above indexes were also significantly increased in C group (P<0.05 or P<0.01).

CONCLUSION: Large V(T) mechanical ventilation can significantly activate the p-p38 and inflammatory cytokines, which may play an important role in VILI.

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