The mechanism of diesel exhaust particles-induced pulmonary inflammation.

我们已经预先报告了diesel exhaust particles (DEP) impaired endothelium dependentrelaxation . The mechanism of The impairment of EDR by DEP was investigated in this study我们包含DEP scavenged NO from endothelium to block its physiological action on smooth超oxide anion radical (o_2) from DEP appears to exert scavenging effect of NO,andperoxynitrite will be produced.When DEP were intratracheally administered to rat, macrophagesneutrophils,lymphocytes and eosinophils migrated in alveoli. Protein concentration in broncho-alveolar lavagefluid （BALF）有时是increased.这些影响suggested that intratracheal administration of DEPinduced pulmonary inflammation. Cells (macrophages and neutrophils) in BALF from DEP administeredrat produced peroxynitrite. peroxynitrite production was increased by 12-O-tetradecanoylphorbol-13-acetate （TPA）刺激which stimulate o_2 - formation in those cells. This result indicated that o_2 - from DEP increasedperoxynitrite formation in alveoli. However cells in BALF from control rat did not生产peroxynitrite before and after TPA stimulation.In conclusion，DEP-induced pulmonary inflammation mechanism of the formation ofperoxynitrite formed by nitric oxide from cells in BALF and o_2 - from cells in BALF and DEP.The效应DEP to scavenge NO from endothelium may also involve DEP-induced pulmonary inflammation byinhibiting the action of NO for anti-inflammatory effects

We have previously reported that diesel exhaust particles (DEP) impaired endothelium dependent relaxation (EDR). The mechanism of the impairment of EDR by DEP was investigated in this study, and we concluded that DEP scavenged NO from endothelium to block its physiological action on smooth muscle. Superoxide anion radical (O_2・-) from DEP appears to exert scavenging effect of NO,and peroxynitrite will be produced.When DEP were intratracheally administered to rat, macrophages, neutrophils, lymphocytes and eosinophils migrated in alveoli. Protein concentration in broncho-alveolar lavage fluid (BALF) was also increased. These results suggested that intratracheal administration of DEP induced pulmonary inflammation. Cells (macrophages and neutrophils) in BALF from DEP administered rat produced peroxynitrite. Peroxynitrite production was increased by 12-O-tetradecanoyl phorbol-13-acetate (TPA) stimulation, which stimulate O_2・- formation in those cells. This result indicated that O_2・- from DEP increased peroxynitrite formation in alveoli. However cells in BALF from control rat did not produce peroxynitrite before and after TPA stimulation.In conclusion, the mechanism of DEP-induced pulmonary inflammation is responsible for the formation of peroxynitrite formed by nitric oxide from cells in BALF and O_2・- from cells in BALF and DEP.The effect of DEP to scavenge NO from endothelium may also involve DEP-induced pulmonary inflammation by inhibiting the action of NO for anti-inflammatory effects.