Effect of particulate matter 2.5 on acute lung injury fibrosis in rats

Abstract

Objective To investigate the effect and mechanism of particulate matter 2.5 (PM2.5) on acute lung injury and pulmonary fibrosis in healthy rats. Methods Sixty healthy Sprague-Dawley (SD) rats were instilled into trachea with two different solutions twice per week for four weeks: Control group with saline and experimental group with PM2.5 60 mg/kg. Experimental subgroup d5 rats were killed 5 days later and subgroup d28 rats 28 days later, respectively. Bronchoalveolar lavage fluid (BALF) were left for measurement of interleukin(IL)-6, tumor necrosis factor-α (TNF-α), type Ⅰ procollagen N-terminal propeptide (PⅠNP) and PⅢNP concentration, right lungs were left for hematoxylin eosin(HE) and Masson dyeing to observe the degree of inflammatory cell infiltration and collagenous fiber distribution, respectively. Results Compared to the control group, the concentration of IL-6 and TNF-α in two experimental groups were significantly higher(P<0.01 or P<0.05); While the level of IL-6 and TNF-α in subgroup d28 was significantly lower than that in subgroup d5(P<0.01 and P<0.05, respectively). The concentration of PⅠNP and PⅢNP in subgroup d5 was significantly higher than that in control group(P<0.05). The levels of PⅠNP and PⅢNP in subgroup d28 were significantly higher than that in the other two groups (P<0.01). Light microscope showed the apparent inflammatory cell infiltration in the lungs of subgroup d5, which was also appeared in subgroup d28. Beyond that, collagenous fiber deposition and pulmonary interstitial fibrosis was also found in subgroup d28. Conclusions PM2.5 inhalation can induce the increase of concentration of inflammatory factors and fibrosis indicators in healthy rats, which leads to the acute lung injury and pulmonary fibrosis. Key words: Particulate matter/AE; Respiratory distress syndrome, adult/ET; Pulmonary fibrosis/ET