The mechanism of diesel exhaust particles-induced pulmonary inflammation.

We have previously reported that diesel exhaust particles （DEP） impaired endothelium dependent relaxation （EDR）DEP对EDR的影响机制被调查在本研究中，我们将DEP从内酯中清除不，以阻止其对平滑肌肉的生理作用结合在一起。来自超氧化物阴离子自由基（O_2·-）的DEP出现了明显清除NO的影响，而过氧化物酶将产生;当DEP被肠道管理为大鼠、宏观、中性、淋巴细胞和碘化的物质时，DEP被移植到阿尔法里。在溴-阿尔维奥拉橡胶流体（BALF）中的蛋白质浓缩也增加了。这些结果被认为是DEP诱导的脉冲炎症管理局的结果。BALF中的细胞（宏观和营养素）来自DEP管理的大鼠生产的过氧化物酶。过氧化物酶的生产由12-O-四十二烷醇酚-13-乙酸酯（TPA）刺激产生，刺激O_2·-在这些细胞中形成。这一结果指示O_2·-来自Alveoli中的DEP增加了过氧化物酶。在TPA刺激之前和之后，BALF中的细胞没有产生过氧化物酶反应。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-炎症效应。

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.