Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sivelestat sodium hydrate (sivelestat) is a selective inhibitor of polymorphonuclear leukocyte elastase (PMN-E). We administered sivelestat to patients with septic acute lung injury (ALI) to examine its usefulness. The primary endpoints in the study were the duration of artificial ventilation and pulmonary oxygenation ability, and the secondary endpoints were mortality and the concentrations of PMN-E, SP-D, TNF-alpha and IL-8 in blood. In the sivelestat group, the duration of artificial ventilation, pulmonary oxygenation ability, and the blood PMN-E, SP-D, TNF-alpha and IL-8 concentrations decreased significantly. Administration of sivelestat was found to reduce alveolar dysfunction and improve respiratory function, and it was suggested that early administration might be useful.
Res Commun Mol Pathol Pharmacol 2006
PMID:Sivelestat sodium hydrate improves septic acute lung injury by reducing alveolar dysfunction. 1797 96

In this study, we irradiated the murine lung and analyzed the inhibitory effects of sivelestat sodium hydrate, a neutrophil elastase (NE) inhibitor, on lung injury in mice. Sivelestat sodium hydrate (3 mg/kg) was administered by intraperitoneal injection immediately, 3, 6, and 12 h after irradiation in groups RE-0, RE-3, RE-6, and RE-12, respectively. A control group and a group receiving radiation without sivelestat (group R) were also used. NE activity was measured 24 and 48 h after irradiation. The lungs were simultaneously extirpated and stained with hematoxylin and eosin and a naphthol AS-D chloroacetate esterase stain (N-ASDCLA). NE activity increased in the groups in which the murine lungs were irradiated. There was no increase in NE activity in the control group. Among the sivelestat-administered groups, NE activity was slightly elevated in group RE-0 and was suppressed, compared to group R, in groups RE-3, RE-6, and RE-12 at 24 h after irradiation. In the irradiated groups, intra-alveolar neutrophil infiltration, perivascular edema, and alveolar wall thickness were observed, but these changes were mild in the sivelestat-administered groups. The number of N-ASDCLA-positive cells increased in the sivelestat-administered groups, while group R had low values. This indicated that sivelestat sodium hydrate blocked the release of NE from the neutrophils in the irradiated lungs. NE plays an important role in the development of radiation-induced lung injury. Sivelestat is thus expected to decrease radiation-induced lung toxicity by suppressing NE release from neutrophils.
Int J Mol Med 2007 Dec
PMID:Effects of sivelestat sodium hydrate on the reduction of radiation pneumonitis. 1798 88